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Did you know?
Crohn’s disease is not limited to the gut. Extra-intestinal manifestations (EIMs) such as arthritis, skin rashes like erythema nodosum, and eye inflammation (uveitis) are common in up to 25% of Crohn’s patients. These EIMs complicate treatment and require coordinated care across multiple specialties.

Crohn’s Disease

Researched by:

  • Divine Aleru ID
    Divine Aleru

    User avatarI am a biochemist with a deep curiosity for the human microbiome and how it shapes human health, and I enjoy making microbiome science more accessible through research and writing. With 2 years experience in microbiome research, I have curated microbiome studies, analyzed microbial signatures, and now focus on interventions as a Microbiome Signatures and Interventions Research Coordinator.

    Read More

December 15, 2025

Crohn’s disease is a chronic inflammatory condition of the gastrointestinal tract that can cause a wide range of symptoms, including abdominal pain, diarrhea, and fatigue. The exact cause of the disease remains unclear, but it is believed to result from a combination of genetic predisposition and environmental factors. Although there is no cure, ongoing advancements in medical research continue to improve management strategies and quality of life for those affected by Crohn’s disease.

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Researched by:

  • Divine Aleru ID
    Divine Aleru

    User avatarI am a biochemist with a deep curiosity for the human microbiome and how it shapes human health, and I enjoy making microbiome science more accessible through research and writing. With 2 years experience in microbiome research, I have curated microbiome studies, analyzed microbial signatures, and now focus on interventions as a Microbiome Signatures and Interventions Research Coordinator.

    Read More

Last Updated: 2025-12-15

Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.

See full history

Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.

Overview

Crohn’s disease (CD) is a chronic, relapsing inflammatory bowel disease characterized by patchy, transmural inflammation that can affect any part of the gastrointestinal tract from the mouth to the anus. Pathologically, it often features non-caseating granulomas and segmental “skip” lesions, distinguishing it from the continuous lesions of ulcerative colitis.[1] CD is now understood as a systemic, immune-mediated condition triggered by an abnormal host immune response to the intestinal microbiome in a genetically susceptible individual.[2] Its complex pathophysiology involves a convergence of factors, including susceptibility genes, gut microbiota dysbiosis, epithelial barrier dysfunction, and environmental triggers, that together drive chronic mucosal inflammation.[3][4] The incidence of Crohn’s disease has risen globally, especially in newly industrialized regions, highlighting the influence of modern environmental and lifestyle factors on disease emergence.[5]

Associated Conditions

Crohn’s disease is a systemic inflammatory disorder that not only affects the gastrointestinal tract but also has widespread effects on other organ systems. Within the gastrointestinal system, CD can lead to various complications such as strictures, fistulas, abscesses, and intestinal perforations.[6][7] These complications arise due to the chronic inflammation of the intestinal wall, which can lead to scarring, deep tissue damage, and abnormal connections between parts of the intestine or between the intestine and other organs. CD is also associated with extraintestinal manifestations (EIMs) like arthritis, uveitis, and skin conditions such as erythema nodosum and pyoderma gangrenosum.[8] Patients with Crohn’s disease also face an increased risk of metabolic and nutritional complications, including malabsorption, malnutrition, and deficiencies in essential vitamins and minerals (e.g., vitamin B12, iron).[9] Conditions like primary sclerosing cholangitis and autoimmune hepatitis are also seen in some CD patients, highlighting the disease’s systemic nature.[10]

What conditions are associated with Crohn's Disease?
Ankylosing Spondylitis (AS) and Spondyloarthritis

Inflammatory arthritis of the spine and sacroiliac joints – part of the axial spondyloarthritis spectrum – is the most common extraintestinal manifestation of Crohn’s disease.[11] Up to about one-quarter of IBD patients experience arthritic complications, including peripheral arthritis and AS.[12] Crohn’s and AS share substantial genetic overlap and immune pathways; in fact, they share more susceptibility loci with each other than any other IBD comorbidity. Both conditions are strongly tied to overactive Th17/IL-23 immune responses, and notably HLA-B27 (a genetic marker associated with AS) positive individuals with IBD are prone to sacroiliitis.[13] Mechanistic links via the microbiome have been proposed: for example, the hypothesis that Klebsiella pneumoniae from the gut may trigger reactive arthritis in genetically predisposed hosts (molecular mimicry) is supported by studies finding elevated anti-Klebsiella antibodies in subjects with AS and Crohn’s.[14]

Psoriasis

Psoriatic skin disease occurs at higher rates in IBD patients than in the general population. Crohn’s disease and psoriasis cluster in families and often co-manifest, reflecting common immune and genetic underpinnings.[15] Notably, genome-wide studies have identified at least 11 susceptibility loci shared between psoriasis and IBD, with four loci (including IL23R, IL12B, REL, and TYK2) showing especially strong overlap for Crohn’s disease.[16][17] Both conditions are driven by dysregulated Th17-cytokine activity, and therapies targeting these pathways are effective in both psoriasis and Crohn’s. The “gut–skin axis” concept suggests that intestinal dysbiosis and inflammation in Crohn’s may promote systemic immune changes that manifest in the skin. Conversely, some patients develop psoriasis as a side effect of IBD medications (e.g. anti-TNF therapy), further indicating intertwined immune mechanisms.[18]

Primary Sclerosing Cholangitis (PSC)

PSC is a fibroinflammatory cholangiopathy of the bile ducts that co-occurs in a subset of IBD patients. In Crohn’s disease, PSC is relatively rare, but its presence signifies a distinct clinical phenotype.[19] PSC–IBD exemplifies the gut–liver axis: patients with PSC and IBD harbor a distinct gut microbiome composition compared to IBD patients without PSC.[20]

Arthritis

Peripheral arthritis is another common extraintestinal manifestation of Crohn’s disease, affecting the large joints (such as knees, hips, and ankles).[21] The inflammation can be either asymmetrical or symmetrical, and in some cases, it may resolve with improvement of the gut symptoms. It is usually managed with NSAIDs, corticosteroids, and biologics.

Uveitis

Uveitis is inflammation of the middle layer of the eye (uvea). It is one of the most common ocular complications in Crohn’s disease, often associated with flare-ups of gastrointestinal symptoms.[22] Uveitis can lead to pain, blurred vision, and sensitivity to light. It is typically managed with corticosteroids or immunosuppressive agents.

Erythema Nodosum

Erythema nodosum is a type of inflammatory skin condition that causes painful, red, raised bumps, usually on the shins.[23] It is a common extraintestinal manifestation in Crohn’s disease and often correlates with active disease or flare-ups. Treatment typically involves managing the underlying disease and using anti-inflammatory medications.

Pyoderma Gangrenosum

Pyoderma gangrenosum is a rare, severe skin disorder that leads to the formation of deep, ulcerative lesions, most commonly on the legs. It is more commonly seen in patients with Crohn’s disease compared to other IBDs.[24] It is often treated with corticosteroids, immunosuppressive agents, or biologic therapies to control both the skin lesions and the underlying inflammation.

Autoimmune Hepatitis

Autoimmune hepatitis is a chronic liver condition where the immune system attacks liver cells, causing inflammation and potentially leading to cirrhosis. This condition can occur in patients with Crohn’s disease and may present with elevated liver enzymes, jaundice, and fatigue.[25] Treatment typically involves corticosteroids and immunosuppressive drugs.

Thromboembolism

Crohn’s disease patients, particularly those with active disease, have an increased risk of venous thromboembolism (VTE), including deep vein thrombosis (DVT) and pulmonary embolism (PE).[26] This is partly due to inflammation-related changes in clotting factors and increased blood viscosity. Anticoagulation therapy may be necessary for management in affected individuals.

Nephrolithiasis

Crohn’s patients, especially those with small bowel involvement or those who have had surgery (e.g., ileal resection), are at an increased risk of developing kidney stones.[27] Adequate hydration and dietary changes are the primary preventive measures.

Osteoporosis and Osteopenia

Due to chronic inflammation, corticosteroid use, and malabsorption of key nutrients (such as calcium and vitamin D), Crohn’s disease patients are at increased risk of developing osteoporosis and osteopenia.[28]

Causes / Causal Theories

Crohn’s disease is believed to result from a confluence of genetic, microbial, immunologic, and environmental factors, rather than a single cause.[29] In a genetically predisposed host, triggers in the environment (such as dietary changes or infections) may disrupt the gut microbiome and mucosal barrier, leading to a maladaptive immune response in the intestine.[30] Several lines of evidence support this multifactorial model and have given rise to several key causal theories. Therapeutic responses highlight the importance of both microbes and immunity: for example, antibiotics targeting bacterial components and immunomodulators like thalidomide (an older drug repurposed for IBD) have both induced remission in Crohn’s patients.[31]

What are the current causal theories of Crohn's Disease?
Genetic Innate-Immune Deficiency

Crohn’s disease is often regarded as a genetically mediated disorder in which susceptibility genes predispose individuals to immune dysregulation. A key theory in understanding the pathogenesis of Crohn’s revolves around mutations in genes responsible for innate immunity. These genes, such as NOD2 (nucleotide-binding oligomerization domain-containing protein 2), ATG16L1 (autophagy related 16-like 1), and IRGM (immunity-related GTPase family M), are involved in recognizing and defending against bacterial components in the gut.[32][33]

For instance, NOD2, a pattern recognition receptor, plays a crucial role in detecting bacterial peptidoglycans.[34] Mutations in this gene are one of the most well-established risk factors for Crohn’s disease, particularly ileal disease. Individuals with these mutations show a reduced ability to clear bacteria in the intestine, leading to microbial dysbiosis (imbalanced gut microbiome) and increased gut inflammation.[35] This immune deficiency causes the body to respond improperly to harmless commensal bacteria, triggering an exaggerated immune response and sustained intestinal inflammation

Microbial Dysbiosis (Pathobiont Overgrowth)

A leading theory in the pathogenesis of Crohn’s disease is microbial dysbiosis, which refers to an imbalance in the gut microbiome that promotes inflammation.[36] In Crohn’s disease, microbiome balance is disrupted, leading to the overgrowth of pathobionts and a reduction in beneficial microbes.[37]

Pathobionts such as Adherent-Invasive Escherichia coli (AIEC) are frequently found in the intestines of Crohn’s patients, particularly in ileal disease, where they invade the intestinal epithelium, persist within macrophages, and promote an inflammatory response.[38] At the same time, beneficial microbes such as Faecalibacterium prausnitzii, a butyrate-producing bacterium, are often depleted in Crohn’s disease.[39] Butyrate plays a crucial role in maintaining intestinal homeostasis by providing energy to colonocytes and modulating immune responses.[40] Its reduction leads to impaired mucosal healing and exacerbates inflammation.

Mycobacterial Infection (MAP Hypothesis)

The Mycobacterium avium subsp. paratuberculosis (MAP) hypothesis posits that Crohn’s disease may be triggered or sustained by an infection with this specific microorganism, which causes Johne’s disease in cattle. MAP has been detected in the intestinal tissues of some Crohn’s patients, leading researchers to speculate that an infection by MAP could initiate the immune response seen in Crohn’s disease.[41]

This theory is grounded in the idea that in genetically susceptible individuals, the immune system’s chronic response to MAP, a bacterium that can survive in macrophages, triggers a cascade of inflammatory responses.[42]

Western Lifestyle and Hygiene Hypothesis

The Western lifestyle and hygiene hypothesis suggest that environmental factors associated with industrialized societies, such as improved sanitation, a Western diet, and reduced childhood infections, have contributed to the rising incidence of Crohn’s disease, particularly in newly industrialized countries.[43] Further supporting this theory, studies have shown that migrants from low-incidence to high-incidence countries tend to adopt the higher risk of their new environment within one or two generations, suggesting that lifestyle factors play a significant role in the development of the disease.[44]

Diagnosis

There is no single test that diagnoses Crohn’s disease at the moment. The accepted diagnostic approach is a combination of clinical evaluation and multiple modalities (“multiple hits”): endoscopic evidence of focal, chronic ulceration (often with normal intervening areas), histological confirmation of chronic active inflammation (with granulomas if present), imaging of the small bowel to assess extent, and exclusion of infections or alternate causes.[45] Newer tools like capsule endoscopy can visualize the small intestine for lesions, and intestinal ultrasound is emerging in some centers as a radiation-free monitoring tool. Once diagnosis is established, clinicians typically classify Crohn’s by location and behavior (using the Montreal or Paris classification), as these have prognostic significance, and they may utilize experimental markers to stratify disease or guide therapy in the future.[46]

Primer

Crohn’s disease is a complex, chronic inflammatory condition primarily affecting the gastrointestinal tract. The disease is driven by a dysregulated immune response to the gut microbiome, leading to chronic inflammation, tissue damage, and complications like strictures and fistulas.[47] Microbial dysbiosis plays a central role in disease initiation and progression, influencing both immune activation and intestinal permeability.[48] Disruptions in metal homeostasis, particularly in trace elements such as zinc and iron, contribute to inflammation and microbial shifts, creating a cycle that perpetuates disease activity.[49][50] The combination of immune system abnormalities, microbiome alterations, and metallomic imbalances underscores the systemic nature of Crohn’s disease, providing a deeper understanding of its pathogenesis and highlighting emerging opportunities for microbiome-based diagnostics and personalized therapies.

Metabolomic Signatures

Crohn’s disease is associated with distinctive shifts in metabolism – many driven by an imbalanced gut microbiome. Patients with CD exhibit broad disturbances in their metabolite profiles, in keeping with the dysbiosis observed in the gut microbiota.[51] In health, gut bacteria produce beneficial compounds (like short-chain fatty acids) and regulate bile acids and amino acids; in Crohn’s, these pathways are often disrupted.[52]

What are the key metabolomic alterations in Crohn's disease?
Short-Chain Fatty Acids (SCFAs)

Levels of SCFAs (e.g. butyrate, acetate), which are normally produced by fiber-fermenting gut bacteria and fuel intestinal cells, are typically reduced in Crohn’s patients.[53] Loss of butyrate-producing taxa (like Faecalibacterium and Roseburia) leads to less butyrate in the colon, impairing mucosal energy supply and anti-inflammatory signaling.[54] This deficiency in SCFAs is linked to a weakened intestinal barrier and dysregulated immune homeostasis.[55]

Succinate

Crohn’s dysbiosis often causes an accumulation of succinate, a microbial fermentation intermediate. In a healthy colon, succinate is usually transient (quickly consumed by other microbes), maintaining very low levels. In active Crohn’s, succinate can build up to millimolar concentrations.[56] Excess succinate is pro-inflammatory – it activates mucosal immune responses via the SUCNR1 receptor, drives macrophage and T-cell metabolic changes, and can stabilize HIF-1α, promoting inflammatory cytokine production.[57] This makes succinate a notable microbiome-derived pro-inflammatory metabolite in CD.

Tryptophan Metabolites

The gut microbiota normally metabolizes tryptophan (an amino acid from diet) into various indoles and other compounds that interact with the host immune system (for example, activating the aryl hydrocarbon receptor to promote regulatory immune pathways). In Crohn’s disease, beneficial tryptophan-derived indoles are often decreased due to loss of key microbes, while other potentially harmful tryptophan metabolites may accumulate.[58]

Bile Acids

Crohn’s disease (especially with ileal involvement) disrupts bile acid metabolism. Normally, gut bacteria transform conjugated primary bile acids (synthesized by the liver) into secondary bile acids. In Crohn’s, a reduction in bile acid-transforming microbes leads to an overabundance of primary bile acids and a depletion of certain secondary bile acids in the intestines.[59] Studies have found that fecal samples from IBD patients have increased conjugated primary bile acids and markedly lower levels of secondary bile acids like deoxycholic acid (DCA) and lithocholic acid (LCA).[60] These changes can affect inflammation – for example, some secondary bile acids have anti-inflammatory or regulatory effects in the gut, and their deficiency may perpetuate intestinal inflammation. Meanwhile, excess primary bile acids in the colon can irritate the mucosa and contribute to diarrhea.

Metallomic Signatures

Trace metal imbalances are a hallmark of Crohn’s disease, arising from both malabsorption and the body’s own immune responses that alter metal distribution. Zinc, iron, and copper in particular show disturbed levels in Crohn’s patients, and these imbalances influence both host immunity and the gut microbial ecosystem. Crohn’s disease entails significant disturbances in trace metals: iron and zinc are sequestered by the host to inhibit microbes, leading to deficiencies, while certain bacteria deploy strategies to acquire these metals, influencing microbial composition. These imbalances (or “mismetalation”) impact disease pathogenesis.

What are the metallomic signatures of Crohn's disease
Iron

Iron deficiency is very common in Crohn’s disease due to chronic intestinal blood loss and reduced absorption (especially if the duodenum is bypassed or inflamed). Many patients develop iron deficiency anemia.[61] Paradoxically, during active inflammation the body increases production of hepcidin (an inflammatory hormone) which locks iron away in storage sites, lowering serum iron.[62] While this helps limit bacterial growth, it worsens anemia. In the gut lumen, low iron availability can shift microbial populations: pathogens like E. coli often have competitive advantages in low-iron environments by producing high-affinity siderophores (iron-scavenging molecules).[63] Indeed, Crohn’s-associated adherent-invasive E. coli (AIEC) secrete siderophores (e.g. enterobactin and yersiniabactin) to capture iron and other metals, allowing them to thrive during inflammation.[64] These E. coli can evade host iron-sequestration defenses – for example, the host releases Lipocalin-2 to bind enterobactin, but AIEC often produce “stealth” siderophores like yersiniabactin that Lipocalin-2 cannot neutralize.[65] The result is a metallomic milieu in Crohn’s wherein iron is scarce for commensals but accessible to pathogens with specialized iron uptake systems.

Zinc

Zinc levels are frequently low in Crohn’s patients as well. Causes include malabsorption (especially with small bowel disease), high intestinal losses, and poor dietary intake.[66] Zinc is critical for immune function and epithelial healing; deficiency can impair gut barrier repair and immune cell function. However, during intestinal inflammation the body actively sequesters zinc as a defense: neutrophils release calprotectin, a protein that binds and removes zinc (and manganese).[67] This zinc withholding is another aspect of nutritional immunity, by limiting zinc, the host tries to inhibit bacterial growth (many microbes need zinc to survive). A side effect is that systemic zinc levels drop. Meanwhile, certain bacteria have evolved mechanisms to acquire zinc despite host defenses. For example, yersiniabactin not only chelates iron but can bind zinc and copper as well, potentially helping AIEC and other pathogens scavenge these metals in the inflamed gut.[68][69] The net effect in Crohn’s is a distorted zinc distribution: low serum zinc, high fecal zinc bound to calprotectin, and microbial competition for any available zinc. This mismetalation can worsen inflammation – zinc deficiency weakens antioxidant defenses and barrier integrity, yet excess free zinc in the gut (if supplementation is overdone) might fuel pathobionts.

Copper

In active Crohn’s, serum copper is often elevated as part of the acute phase response, the liver increases production of ceruloplasmin during inflammation, raising copper levels in blood. Consequently, the copper-to-zinc ratio in plasma tends to be high in active IBD, and this ratio correlates with disease activity (higher ratio with more inflammation).[70] Despite high serum copper, Crohn’s patients can experience functional copper deficiency if malabsorption is severe (since copper is absorbed in the upper small intestine). [71]Low copper could contribute to anemia (copper is needed for iron metabolism) and neutropenia, though overt copper deficiency is less common than iron or zinc deficits.[72] From a microbial standpoint, copper is a double-edged sword: it is an essential micronutrient but also toxic in excess. The host immune system sometimes exploits copper’s toxicity by pumping copper into phagolysosomes to kill bacteria.[73] Some gut bacteria (like Enterococcus faecalis or E. coli) carry copper export pumps or resistance genes to survive; an imbalance in copper might thus alter which microbes flourish.[74]

Nutritional Immunity and Supplementation Paradoxes

The concept of nutritional immunity, which is the host’s strategy of withholding nutrients (like metals) to combat pathogens, is key to understanding some paradoxical findings in Crohn’s disease.[75] The immune system actively alters nutrient availability during inflammation: as noted, it hides away iron and zinc, creating an unfriendly environment for bacteria. This is beneficial in controlling infection, but in Crohn’s, it also contributes to micronutrient deficiencies. Attempts to correct these deficiencies through supplementation can yield unexpected results, sometimes worsening inflammation or dysbiosis if not done carefully. Nutritional immunity and Crohn’s create a delicate balance: the body’s efforts to protect itself by sequestering nutrients can lead to deficiencies, and reversing those deficiencies isn’t as simple as giving high-dose supplements.

What Nutritional Immunity factors and paradoxes in Crohn's disease?
Iron Supplementation

Iron is needed to treat Crohn’s-related anemia, yet giving iron (especially orally) can aggravate the disease. Excess free iron in the gut can catalyze the formation of reactive oxygen species (via Fenton reactions), increasing oxidative stress in the already inflamed intestinal lining.[76] Moreover, additional luminal iron may feed pro-inflammatory bacteria – E. coli and other opportunists bloom when iron is abundant, potentially exacerbating dysbiosis.[77] Clinical studies have observed that oral iron can elevate fecal calprotectin (an inflammation marker) and disrupt the microbiota in IBD patients.[78] In fact, the need for iron repletion “exacerbates the dysbiosis” in Crohn’s, creating a vicious cycle. To navigate this, current practice often favors intravenous iron for Crohn’s patients with active disease, delivering iron directly to the bloodstream restores levels without flooding the gut with iron.[79] This approach avoids feeding gut microbes and bypasses the inflamed intestinal absorption pathways. Thus, the paradox is that while iron is essential to the patient, in the context of an inflamed gut more iron can mean more inflammation.

Zinc Supplementation

Zinc deficiency can impair wound healing and immunity, so one might assume supplementing zinc would always be helpful in Crohn’s. However, excess zinc can have adverse effects. In a mouse study of C. difficile-associated colitis, for example, excess dietary zinc worsened inflammation and disease severity.[80] The mechanism relates to nutritional immunity: normally, calprotectin from neutrophils binds zinc to keep it away from pathogens like in colitis.[81] If the diet massively increases zinc, this host defense can be overwhelmed, leaving more free zinc for pathogens and disrupting the normal microbial balance. So, despite low serum zinc in Crohn’s being linked to worse outcomes (and supplementation often being necessary), giving large doses of zinc might paradoxically fuel intestinal inflammation in some contexts.

Microbiome Signature: Crohn’s Disease

Interventions

Beyond conventional therapies, a range of emerging and non-mainstream interventions are being explored for Crohn’s disease – often aiming to target the microbiome, dietary factors, or novel pathways of inflammation. Given the central role of gut bacteria in Crohn’s, therapies that alter the microbiome are a major focus. These approaches are in early clinical trials or have mechanistic support in research.

What novel interventions exist for Crohn's disease?
Bacteriophage therapy

This involves using viruses that infect bacteria to selectively eliminate harmful microbes. For instance, researchers have developed phage cocktails targeting Adherent-Invasive Escherichia coli (AIEC). In mouse models, orally administered phages against AIEC significantly reduced the burden of these bacteria and alleviated intestinal inflammation.[82] These findings have led to early-phase clinical trials of AIEC-targeted phage therapy in Crohn’s patients.[83] The goal is to “rebalance” the microbiome by removing a pathogenic strain without broad antibiotics – a narrow-spectrum antimicrobial approach

Narrow-spectrum antibiotics

These would suppress specific pro-inflammatory microbes (such as Fusobacterium or E. coli) while sparing beneficial flora. One example is anti-MAP therapy, a combination antibiotic regimen aimed at Mycobacterium avium paratuberculosis, a bacterium hypothesized to trigger Crohn’s in some patients, although results have been mixed.[84]

Hyperbaric Oxygen Therapy (HBOT)

In HBOT, patients breathe 100% oxygen in a high-pressure chamber, has shown promise for difficult Crohn’s cases. The idea is that flooding tissues with oxygen aids healing of chronic wounds and reduces inflammation (hypoxia in gut tissues is thought to drive inflammation).[85] There is evidence that HBOT can help heal complex perianal fistulas and reduce Crohn’s disease activity in refractory patients.[86] For perianal Crohn’s, where options are limited, HBOT achieved notable fistula closure rates in some studies.[87] It is considered safe and is usually used as an adjunct to standard therapy in research settings.

In addition to the Phase 2–3 trials in Crohn’s, a wave of therapies that target specific immune and microbial pathways is being brought forward: IL-23 p19 inhibitors and S1P modulators are leading the pack with positive trial results, and others like JAK inhibitors and novel biologics are close behind.[88] The hope is that within the next few years, these will expand the toolkit for Crohn’s, allowing more personalized and effective treatment regimens.

FAQs

Is Crohn’s disease curable?

At present, Crohn’s disease cannot be cured – not in the sense of eliminating it forever. It is a chronic (lifelong) condition. However, it can be brought into remission and kept there for long periods, during which a person may feel completely well. The goal of therapy is exactly that: lasting remission and healing of the intestines. Some patients achieve remission that lasts many years, especially with effective treatment and lifestyle adjustments, but the underlying tendency for inflammation is still there, meaning flares can occur if treatment is withdrawn or due to unknown triggers. Unlike ulcerative colitis, Crohn’s usually cannot be cured by surgery either. In UC, removing the colon essentially cures the disease (albeit at the cost of losing the colon). In Crohn’s, surgery can remove diseased sections, but the inflammation often returns at the margins of where the tissue was removed or in other GI locations (for example, after an ileal resection, many patients get recurrence at the new ileocolonic junction). There are cases of clinical cure – someone has surgery and never has issues again, or very mild disease controlled with minimal meds – but this is more the exception than the rule. The chronic nature also relates to its autoimmune character; like other autoimmune diseases (rheumatoid arthritis, etc.), Crohn’s tends to require ongoing management. The encouraging news is that with modern treatments, many patients achieve deep remission (no symptoms, normal lab tests, healed mucosa on colonoscopy). Some are effectively “disease-free” while on therapy, which raises the question: if you’ve been in remission 10+ years on a biologic, are you essentially cured as long as you continue the drug? It’s a semantic point – the disease is controlled but not eradicated. Researchers are searching for cures, possibly through early intervention, resetting the immune system, or targeted microbial therapies, but so far, no intervention has reliably cured Crohn’s. Therefore, patients and doctors focus on control, not cure: using medication, diet, sometimes surgery, and other strategies to keep the disease in check such that the person can live a full, healthy life. It’s worth noting that the vast majority of Crohn’s patients can live normal lifespans, and many have long stretches of good health – so while it isn’t “curable” today, it is very treatable.

Is Crohn’s disease caused by stress?

Crohn’s is not caused by stress. It is a biological disease of the immune system and gut, driven by factors like genetics, intestinal microbiome, and environmental triggers (such as smoking or perhaps diet). However, stress can influence Crohn’s symptoms and possibly trigger flares in someone who already has the disease. Many patients report that during times of high stress (e.g. major life events, anxiety, etc.), their digestive symptoms worsen. Stress can affect gut motility, permeability, and the immune system (via stress hormones), which might exacerbate inflammation or make one more susceptible to a flare-up. But it’s important to understand that Crohn’s is not a psychosomatic illness – you do not get Crohn’s because you were under stress, and conversely, a calm life will not completely prevent Crohn’s if the underlying disease process is there. In the mid-20th century, Crohn’s (and ulcerative colitis) were at times thought to be “stress-related” illnesses; we now know that while mind-gut interactions are real, the root causes lie in immune dysregulation and gut flora. Bottom line: Stress is considered a modulating factor, not the primary cause. Managing stress through mindfulness, therapy, or relaxation techniques can be a helpful part of comprehensive care (since it may improve one’s overall well-being and potentially reduce symptom frequency), but it cannot replace medical treatment for the inflammation. Patients should feel reassured that Crohn’s is not “their fault” for being stressed – it’s an organic disease. That said, good stress management and mental health care are an important adjunct since living with a chronic illness can itself be stressful, creating a cycle that’s worth breaking.

What is the difference between Crohn’s disease and ulcerative colitis?

Crohn’s disease and ulcerative colitis (UC) are the two main forms of inflammatory bowel disease, but they affect the gut differently. Crohn’s can involve any part of the gastrointestinal tract from mouth to anus, often in a patchy “skip lesion” distribution, and inflammation goes through the entire wall of the bowel. This means Crohn’s can cause strictures, deep ulcers, and fistulas (tunnels to other organs). Ulcerative colitis, by contrast, is limited to the colon and rectum and is continuous (starting at the rectum and extending upward) – it only affects the innermost mucosal layer of the colon. So UC causes superficial ulcers and bleeding in the colon but typically not fistulas or thick scarring. In terms of symptoms, both can cause abdominal pain and diarrhea, but UC more often has bloody diarrhea, whereas Crohn’s might have more variable symptoms (sometimes fatty diarrhea if the small bowel is involved, weight loss, nutritional deficiencies, etc.). Systemic features like fevers and weight loss occur in both, but are often pronounced in Crohn’s when the small intestine is affected leading to malabsorption. Another difference is seen in endoscopy: Crohn’s has a cobblestone appearance with normal areas between patches of disease, while UC has a uniform, diffuse inflammation. Pathology can also distinguish them (Crohn’s has granulomas on biopsy ~ in some cases, and UC does not, and UC has crypt abscesses in the mucosa). Distinguishing Crohn’s from UC is important because it affects treatment (for example, surgery can potentially cure UC by removing the colon, but in Crohn’s, surgery is not curative because disease can recur elsewhere).

Research Feed

Diagnostic Procedures for Inflammatory Bowel Disease: Laboratory, Endoscopy, Pathology, Imaging, and Beyond
June 28, 2024
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Crohn’s Disease
Crohn’s Disease

Did you know?
Crohn’s disease is not limited to the gut. Extra-intestinal manifestations (EIMs) such as arthritis, skin rashes like erythema nodosum, and eye inflammation (uveitis) are common in up to 25% of Crohn’s patients. These EIMs complicate treatment and require coordinated care across multiple specialties.

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Crohn’s Disease: Evolution, Epigenetics, and the Emerging Role of Microbiome-Targeted Therapies
February 23, 2016
/
Crohn’s Disease
Crohn’s Disease

Did you know?
Crohn’s disease is not limited to the gut. Extra-intestinal manifestations (EIMs) such as arthritis, skin rashes like erythema nodosum, and eye inflammation (uveitis) are common in up to 25% of Crohn’s patients. These EIMs complicate treatment and require coordinated care across multiple specialties.

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Novel Insights into the Pathogenesis of Inflammatory Bowel Diseases
January 25, 2025
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Crohn’s Disease
Crohn’s Disease

Did you know?
Crohn’s disease is not limited to the gut. Extra-intestinal manifestations (EIMs) such as arthritis, skin rashes like erythema nodosum, and eye inflammation (uveitis) are common in up to 25% of Crohn’s patients. These EIMs complicate treatment and require coordinated care across multiple specialties.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Epithelial barrier dysfunction and microbial dysbiosis in Crohn’s disease
August 26, 2024
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Environmental risk factors of inflammatory bowel disease: toward a strategy of preventative health
March 11, 2025
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

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Intestinal Stricture in Crohn’s Disease
January 29, 2015
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Clinical Features of Intra-Abdominal Abscess and Intestinal Free-Wall Perforation in Korean Patients with Crohn’s Disease
December 30, 2020
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Extraintestinal Manifestations in Inflammatory Bowel Disease: From Pathophysiology to Treatment
August 12, 2024
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Nutritional Status and Its Detection in Patients with Inflammatory Bowel Diseases
April 20, 2023
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

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Prevalence and Bidirectional Association Between Autoimmune Liver Disease and Inflammatory Bowel Disease
August 10, 2025
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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The Link between Ankylosing Spondylitis, Crohn’s Disease, Klebsiella, and Starch Consumption
May 27, 2013
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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New developments in our understanding of ankylosing spondylitis pathogenesis
July 22, 2020
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Psoriasis and inflammatory bowel disease: links and risks
July 20, 2016
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Psoriasis as a Potential Risk Factor for Inflammatory Bowel Disease (IBD)
September 23, 2025
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Incidence of and Risk Factors for Paradoxical Psoriasis or Psoriasiform Lesions in Inflammatory Bowel Disease Patients Receiving Anti-TNF Therapy
March 1, 2022
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Primary sclerosing cholangitis and inflammatory bowel disease comorbidity: an update of the evidence
January 15, 2019
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

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Ocular Manifestations of IBD: Pathophysiology, Epidemiology, and Iatrogenic Associations of Emerging Treatment Strategies
December 16, 2024
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Extraintestinal Manifestations of Inflammatory Bowel Disease
February 1, 2008
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Pyoderma gangrenosum and inflammatory bowel disease: Recent insights into epidemiology, pathogenesis, and therapeutic approaches.
November 12, 2025
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Long-term risk of inflammatory bowel disease in autoimmune hepatitis: Over a 20-year population-based study
September 6, 2025
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Thromboembolic Events in Patients with Inflammatory Bowel Disease: A Comprehensive Overview
September 30, 2022
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Nephrolithiasis in Crohn’s Disease Patients: A Review of the Literature
April 1, 2022
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Osteoporosis Complications in Crohn’s Disease Patients: Factors, Pathogenesis, and Treatment Outlines
December 21, 2025
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Genetic and environmental factors influencing Crohn’s disease
March 27, 2025
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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NOD2 in Crohn’s Disease—Unfinished Business
August 25, 2022
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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The Role of Gut Microbiota in Intestinal Inflammation with Respect to Diet and Extrinsic Stressors
August 19, 2019
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Advancements in Immunomodulatory Therapies for IBD and Their Interplay With the Gut–Brain Axis
August 10, 2025
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Genetic and Epigenetic Etiology of Inflammatory Bowel Disease: An Update
December 16, 2022
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Microbial dysbiosis in the gut drives systemic autoimmune diseases
October 20, 2022
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Gut microbiota dysbiosis in inflammatory bowel disease: Interaction with intestinal barriers and microbiota-targeted treatment options
June 27, 2025
/

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Mycobacterium avium subspecies paratuberculosis (MAP) and Crohn’s disease: the debate continues
July 25, 2023
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Mycobacterium avium subspecies paratuberculosis and its relationship with Crohn’s disease
January 28, 2009
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Environmental Influences on the Onset and Clinical Course of Crohn’s Disease
November 1, 2013
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Epidemiological studies of migration and environmental risk factors in the inflammatory bowel diseases
February 7, 2014
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Artificial intelligence-assisted capsule endoscopy for detecting lesions in Crohn’s disease
April 1, 2025
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Crohn’s disease and clinical management today: How it does?
December 20, 2023
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Homeostasis and Inflammation in the Intestine
March 19, 2010
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Microbiome-metabolome generated bile acids gatekeep infliximab efficacy in Crohn’s disease
August 12, 2025
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Metabolic Influences of Gut Microbiota Dysbiosis on Inflammatory Bowel Disease
September 27, 2021
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Succinate’s Dual Roles in Inflammatory Bowel Disease
October 28, 2025
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Succinate metabolism: underlying biological mechanisms and emerging therapeutic targets in inflammatory bowel disease
September 10, 2025
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Relationship between the gut microbiota and bile acid composition in the ileal mucosa of Crohn’s disease
May 14, 2021
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Altered fecal bile acid composition in active ulcerative colitis
November 18, 2023
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Iron Deficiency Anemia: An Overlooked Complication of Crohn’s Disease
April 12, 2022
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Siderophore-mediated iron acquisition and modulation of host-bacterial interactions
October 27, 2016
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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The Prevalence of Zinc Deficiency in Crohn’s Disease Patients
March 1, 2021
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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The Copper/Zinc Ratio Correlates With Markers of Disease Activity in Patients With Inflammatory Bowel Disease.
January 23, 2020
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Copper in infectious disease: Using both sides of the penny
January 7, 2021
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Genome sequences of copper resistant and sensitive Enterococcus faecalis strains isolated from copper-fed pigs in Denmark
July 8, 2015
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Nutritional Immunity and Metallomic Signatures: Metal Competition at the Host–Pathogen Interface
Metals
Metals

Lorem ipsum dolor sit amet, consectetur adipiscing elit. Proin ut laoreet tortor. Donec euismod fermentum pharetra. Nullam at tristique enim. In sit amet molestie

Nutritional Immunity
Nutritional Immunity

Nutritional immunity restricts metal access to pathogens, leveraging sequestration, transport, and toxicity to control infections and immunity.

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The effect of iron therapy on oxidative stress and intestinal microbiota in inflammatory bowel diseases: A review on the conundrum
October 30, 2023
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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The role of zinc and nutritional immunity in Clostridium difficile infection
September 25, 2018
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Gut Microbiota: Role in Pathogen Colonization, Immune Responses and Inflammatory Disease
September 1, 2018
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Phage therapy: Targeting intestinal bacterial microbiota for the treatment of liver diseases
September 23, 2023
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Anti-Mycobacterium paratuberculosis (MAP) therapy for Crohn’s disease: an overview and update
July 28, 2020

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The effects of hyperbaric treatment on perianal fistula activity in patients with Crohn’s disease
September 23, 2024
/
Autoimmune Diseases
Autoimmune Diseases

Did you know?
Americans are over three times more likely to suffer from autoimmune diseases compared to the global average, with approximately 16.67% of the U.S. population affected versus 5% worldwide.

Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.

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Update History

2025-11-03 13:04:59

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published

Crohn’s Disease

Crohn's disease is a chronic inflammatory condition of the gastrointestinal tract that can cause a wide range of symptoms, including abdominal pain, diarrhea, and fatigue. The exact cause of the disease remains unclear, but it is believed to result from a combination of genetic predisposition and environmental factors. Although there is no cure, ongoing advancements in medical research continue to improve management strategies and quality of life for those affected by Crohn's disease.

Crohn’s Disease

Crohn's disease is a chronic inflammatory condition of the gastrointestinal tract that can cause a wide range of symptoms, including abdominal pain, diarrhea, and fatigue. The exact cause of the disease remains unclear, but it is believed to result from a combination of genetic predisposition and environmental factors. Although there is no cure, ongoing advancements in medical research continue to improve management strategies and quality of life for those affected by Crohn's disease.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Crohn’s Disease

Crohn's disease is a chronic inflammatory condition of the gastrointestinal tract that can cause a wide range of symptoms, including abdominal pain, diarrhea, and fatigue. The exact cause of the disease remains unclear, but it is believed to result from a combination of genetic predisposition and environmental factors. Although there is no cure, ongoing advancements in medical research continue to improve management strategies and quality of life for those affected by Crohn's disease.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Metals

Heavy metals play a significant and multifaceted role in the pathogenicity of microbial species.

Nutritional Immunity

Nutritional immunity restricts metal access to pathogens, leveraging sequestration, transport, and toxicity to control infections and immunity.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

Autoimmune Diseases

Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.

References

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Hong, Seung M., and Dong H. Baek.

Diagnostic Procedures for Inflammatory Bowel Disease: Laboratory, Endoscopy, Pathology, Imaging, and Beyond.

Diagnostics 14, no. 13 (2024): 1384. Accessed December 6, 2025.

Read Review

DeFilippis, E. M., Longman, R., Harbus, M., Dannenberg, K., & Scherl, E. J. (2016).

Crohn’s disease: Evolution, epigenetics, and the emerging role of microbiome-targeted therapies.

Current Gastroenterology Reports, 18(13), 13.

Read Review

Calvez, V., Puca, P., Vincenzo, F. D., Gaudio, A. D., Bartocci, B., Murgiano, M., Iaccarino, J., Parand, E., Napolitano, D., Pugliese, D., Gasbarrini, A., & Scaldaferri, F. (2025).

Novel Insights into the Pathogenesis of Inflammatory Bowel Diseases.

Biomedicines, 13(2).

Read Review

Akkoç, T. (2024). Epithelial barrier dysfunction and microbial dysbiosis:

Exploring the pathogenesis and therapeutic strategies for Crohn’s disease.

Tissue Barriers, 13(2), 2390705.

Read Review

Chhibba, T., Gros, B., King, J. A., Windsor, J. W., Gorospe, J., Leibovitzh, H., Xue, M., Turpin, W., Croitoru, K., Ananthakrishnan, A. N., Gearry, R. B., & Kaplan, G. G. (2025).

Environmental risk factors of inflammatory bowel disease: Toward a strategy of preventative health.

Journal of Crohn's and Colitis, 19(4).

Read Review

Chang, W., Wong, M., Tung, C., Shih, L., Wang, Y., & Wei, C. (2015).

Intestinal Stricture in Crohn's Disease.

Intestinal Research, 13(1), 19.

Read Review

Jeong, H., Choi, J. S., Kim, J. W., Kim, H. M., Kim, S., Im, J. P., Kim, J. S., Kim, Y. S., Cheon, J. H., Kim, W. H., Ye, B. D., Kim, H., Han, D. S., Jeong, H., Choi, J. S., Kim, J. W., Kim, H. M., Kim, S., Im, J. P., . . . Han, D. S. (2020).

Clinical Features of Intra-Abdominal Abscess and Intestinal Free-Wall Perforation in Korean Patients with Crohn’s Disease: Results from the CONNECT Study.

Journal of Clinical Medicine, 10(1).

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Faggiani, I., Fanizza, J., Allocca, M., Zilli, A., Parigi, T. L., Barchi, A., Danese, S., Furfaro, F., Faggiani, I., Fanizza, J., Allocca, M., Zilli, A., Parigi, T. L., Barchi, A., Danese, S., & Furfaro, F. (2024).

Extraintestinal Manifestations in Inflammatory Bowel Disease: From Pathophysiology to Treatment.

Biomedicines, 12(8).

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Jabłońska, B., & Mrowiec, S. (2023).

Nutritional Status and Its Detection in Patients with Inflammatory Bowel Diseases.

Nutrients, 15(8), 1991.

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Shi, H., Dou, D., Zhang, F., Du, Y., Zhao, L., Zhi, J., & Zhao, L. (2025).

Prevalence and Bidirectional Association Between Autoimmune Liver Disease and Inflammatory Bowel Disease: A Meta-Analysis.

Journal of Gastroenterology and Hepatology, 40(10), 2362-2372.

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Rashid, T., Wilson, C., & Ebringer, A. (2013).

The Link between Ankylosing Spondylitis, Crohn's Disease, Klebsiella, and Starch Consumption.

Clinical and Developmental Immunology, 2013, 872632.

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Faggiani, I., Fanizza, J., Allocca, M., Zilli, A., Parigi, T. L., Barchi, A., Danese, S., Furfaro, F., Faggiani, I., Fanizza, J., Allocca, M., Zilli, A., Parigi, T. L., Barchi, A., Danese, S., & Furfaro, F. (2024).

Extraintestinal Manifestations in Inflammatory Bowel Disease: From Pathophysiology to Treatment.

Biomedicines, 12(8).

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Voruganti, A., & Bowness, P. (2020).

New developments in our understanding of ankylosing spondylitis pathogenesis.

Immunology, 161(2), 94-102.

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Rashid, T., Wilson, C., & Ebringer, A. (2013).

The Link between Ankylosing Spondylitis, Crohn's Disease, Klebsiella, and Starch Consumption.

Clinical and Developmental Immunology, 2013, 872632.

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Vlachos, C., Gaitanis, G., Katsanos, K. H., Christodoulou, D. K., Tsianos, E., & Bassukas, I. D. (2016).

Psoriasis and inflammatory bowel disease: Links and risks.

Psoriasis (Auckland, N.Z.), 6, 73.

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Vlachos, C., Gaitanis, G., Katsanos, K. H., Christodoulou, D. K., Tsianos, E., & Bassukas, I. D. (2016).

Psoriasis and inflammatory bowel disease: Links and risks.

Psoriasis (Auckland, N.Z.), 6, 73.

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Kang, H. S., Han, K. M., Kim, H., Yoo, D. M., Choi, H. G., Kim, N. Y., Min, W., Kwon, M. J., Kang, H. S., Han, K. M., Kim, H., Yoo, D. M., Choi, H. G., Kim, N. Y., Min, W., & Kwon, M. J. (2025).

Psoriasis as a Potential Risk Factor for Inflammatory Bowel Disease: Findings from a Nationally Representative Korean Population.

Biomedicines, 13(10).

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Mertz, A., Nguyen, N. A., Katsanos, K. H., & Kwok, R. M. (2019).

Primary sclerosing cholangitis and inflammatory bowel disease comorbidity: An update of the evidence.

Annals of Gastroenterology, 32(2), 124.

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Quraishi MN, Sergeant M, Kay G, et al

The gut-adherent microbiota of PSC–IBD is distinct to that of IBD

Gut 2017;66:386-388.

Faggiani, I., Fanizza, J., Allocca, M., Zilli, A., Parigi, T. L., Barchi, A., Danese, S., Furfaro, F., Faggiani, I., Fanizza, J., Allocca, M., Zilli, A., Parigi, T. L., Barchi, A., Danese, S., & Furfaro, F. (2024).

Extraintestinal Manifestations in Inflammatory Bowel Disease: From Pathophysiology to Treatment.

Biomedicines, 12(8).

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Richardson, H., Yoon, G., Moussa, G., Kumar, A., & Harvey, P. (2024).

Ocular Manifestations of IBD: Pathophysiology, Epidemiology, and Iatrogenic Associations of Emerging Treatment Strategies.

Biomedicines, 12(12), 2856.

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Jose, F. A., & Heyman, M. B. (2008).

Extraintestinal Manifestations of Inflammatory Bowel Disease.

Journal of Pediatric Gastroenterology and Nutrition, 46(2), 124.

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Downey, K., Zhang, R., & Ortega-Loayza, A. G. (2025).

Pyoderma gangrenosum and inflammatory bowel disease: Recent insights into epidemiology, pathogenesis, and therapeutic approaches.

Journal of Inflammation Research, 18, 15859–15873.

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Tatour, M., Baker, F. A., Saadi, T., & Hazzan, R. (2025).

Long-term risk of inflammatory bowel disease in autoimmune hepatitis: Over a 20-year population-based study.

Clinics and Research in Hepatology and Gastroenterology, 49(8), 102682.

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Gala, D., Newsome, T., Roberson, N., Lee, S. M., Thekkanal, M., Shah, M., Kumar, V., Bandaru, P., & Gayam, V. (2022).

Thromboembolic Events in Patients with Inflammatory Bowel Disease: A Comprehensive Overview.

Diseases, 10(4), 73.

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Trad, G., Chauhan, S., Brockway, M., Diaz, V., & Hatim, G. (2022).

Nephrolithiasis in Crohn’s Disease Patients: A Review of the Literature.

GSC Advanced Research and Reviews, 11(1), 31–36.

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Baban, Y. N., Edicheria, C. M., Joseph, J., Kaur, P., & Mostafa, J. A. (2021).

Osteoporosis Complications in Crohn's Disease Patients: Factors, Pathogenesis, and Treatment Outlines.

Cureus, 13(12), e20564.

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Fan, H., Wang, W., Gao, N., Li, M., & Jiao, Y. (2025).

Genetic and environmental factors influencing Crohn’s disease.

World Journal of Gastrointestinal Surgery, 17(3), 98526.

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Lobionda, S., Sittipo, P., Kwon, H.Y., & Lee, Y.K. (2019).

The Role of Gut Microbiota in Intestinal Inflammation with Respect to Diet and Extrinsic Stressors.

Microorganisms, 7(8), 271.

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Jha, M., Waheed, A., Hooti, J. A., Nair, S., Najam, A., Mal, M., Tummala, N., Shariq, A. S., Hurairah, A., & Daniel, M. (2025).

Advancements in Immunomodulatory Therapies for IBD and Their Interplay With the Gut–Brain Axis: An Updated Review of Current Literature and Beyond.

Health Science Reports, 8(8), e71157.

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Fan, H., Wang, W., Gao, N., Li, M., & Jiao, Y. (2025).

Genetic and environmental factors influencing Crohn’s disease.

World Journal of Gastrointestinal Surgery, 17(3), 98526.

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Ashton JJ, Seaby EG, Beattie RM, Ennis S.

NOD2 in Crohn’s Disease—Unfinished Business.

J Crohn’s Colitis. 2023;17:450-458.

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Ashton JJ, Seaby EG, Beattie RM, Ennis S.

NOD2 in Crohn’s Disease—Unfinished Business.

J Crohn’s Colitis. 2023;17:450-458.

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Jarmakiewicz-Czaja, S., Zielińska, M., Sokal, A., & Filip, R. (2022).

Genetic and Epigenetic Etiology of Inflammatory Bowel Disease: An Update.

Genes, 13(12), 2388.

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Mousa, W. K., Chehadeh, F., & Husband, S. (2022).

Microbial dysbiosis in the gut drives systemic autoimmune diseases.

Frontiers in Immunology, 13, 906258.

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Xie, H., Yu, S., Tang, M., Xun, Y., Shen, Q., & Wu, G. (2025).

Gut microbiota dysbiosis in inflammatory bowel disease: Interaction with intestinal barriers and microbiota-targeted treatment options.

Frontiers in Cellular and Infection Microbiology, 15, 1608025.

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Xie, H., Yu, S., Tang, M., Xun, Y., Shen, Q., & Wu, G. (2025).

Gut microbiota dysbiosis in inflammatory bowel disease: Interaction with intestinal barriers and microbiota-targeted treatment options.

Frontiers in Cellular and Infection Microbiology, 15, 1608025.

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Xie, H., Yu, S., Tang, M., Xun, Y., Shen, Q., & Wu, G. (2025).

Gut microbiota dysbiosis in inflammatory bowel disease: Interaction with intestinal barriers and microbiota-targeted treatment options.

Frontiers in Cellular and Infection Microbiology, 15, 1608025.

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Xie, H., Yu, S., Tang, M., Xun, Y., Shen, Q., & Wu, G. (2025).

Gut microbiota dysbiosis in inflammatory bowel disease: Interaction with intestinal barriers and microbiota-targeted treatment options.

Frontiers in Cellular and Infection Microbiology, 15, 1608025.

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Mintz, M. J., & Lukin, D. J. (2023).

Mycobacterium avium subspecies paratuberculosis (MAP) and Crohn’s disease: The debate continues.

Translational Gastroenterology and Hepatology, 8, 28.

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Mendoza, J. L., Lana, R., & Díaz-Rubio, M. (2009).

Mycobacterium avium subspecies paratuberculosis and its relationship with Crohn’s disease.

World Journal of Gastroenterology : WJG, 15(4), 417.

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Dam, A. N., Berg, A. M., & Farraye, F. A. (2013).

Environmental Influences on the Onset and Clinical Course of Crohn’s Disease—Part 1: An Overview of External Risk Factors.

Gastroenterology & Hepatology, 9(11), 711.

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Ko, Y., Butcher, R., & Leong, R. W. (2014).

Epidemiological studies of migration and environmental risk factors in the inflammatory bowel diseases.

World Journal of Gastroenterology : WJG, 20(5), 1238.

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Hong, Seung M., and Dong H. Baek.

Diagnostic Procedures for Inflammatory Bowel Disease: Laboratory, Endoscopy, Pathology, Imaging, and Beyond.

Diagnostics 14, no. 13 (2024): 1384. Accessed December 6, 2025.

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Bin, Y., Peng, R., Lee, Y., Lee, Z., & Liu, Y. (2025).

Artificial intelligence-assisted capsule endoscopy for detecting lesions in Crohn’s disease: A systematic review and meta-analysis.

Frontiers in Artificial Intelligence, 8, 1531362.

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Júnior, S., Apolonio, J. S., Nascimento, S., Malheiro, L. H., Luz, M. S., & Santos, S. (2023).

Crohn's disease and clinical management today: How it does?

World Journal of Methodology, 13(5), 399.

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Mousa, W. K., Chehadeh, F., & Husband, S. (2022).

Microbial dysbiosis in the gut drives systemic autoimmune diseases.

Frontiers in Immunology, 13, 906258.

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Narvey, S., Ghia, J., Marrie, R. A., Armstrong, H., & Bernstein, C. N. (2025).

Heavy Metals and Inflammatory Bowel Disease.

Gastroenterology, 169(5), 761-766.e2.

Garrett, W. S., Gordon, J. I., & Glimcher, L. H. (2010).

Homeostasis and Inflammation in the Intestine.

Cell, 140(6), 859.

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Liu, L., Liang, L., Liang, H., Wang, M., Zhou, W., Mai, G., Yang, C., & Chen, Y. (2025).

Microbiome-metabolome generated bile acids gatekeep infliximab efficacy in Crohn’s disease by licensing M1 suppression and Treg dominance.

Journal of Advanced Research.

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Sultan, S., El-Mowafy, M., Elgaml, A., E Ahmed, T. A., Hassan, H., & Mottawea, W. (2021).

Metabolic Influences of Gut Microbiota Dysbiosis on Inflammatory Bowel Disease.

Frontiers in Physiology, 12, 715506.

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Sultan, S., El-Mowafy, M., Elgaml, A., E Ahmed, T. A., Hassan, H., & Mottawea, W. (2021).

Metabolic Influences of Gut Microbiota Dysbiosis on Inflammatory Bowel Disease.

Frontiers in Physiology, 12, 715506.

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Xie, H., Yu, S., Tang, M., Xun, Y., Shen, Q., & Wu, G. (2025).

Gut microbiota dysbiosis in inflammatory bowel disease: Interaction with intestinal barriers and microbiota-targeted treatment options.

Frontiers in Cellular and Infection Microbiology, 15, 1608025.

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Lavelle, A., & Sokol, H. (2020).

Gut microbiota-derived metabolites as key actors in inflammatory bowel disease.

Nature Reviews Gastroenterology & Hepatology, 17(4), 223-237.

Bamba, S., Inatomi, O., Nishida, A., Ohno, M., Imai, T., Takahashi, K., Naito, Y., Iwamoto, J., Honda, A., Inohara, N., & Andoh, A. (2022).

Relationship between the gut microbiota and bile acid composition in the ileal mucosa of Crohn’s disease.

Intestinal Research, 20(3), 370–380.

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Sommersberger, S., Gunawan, S., Elger, T., Fererberger, T., Loibl, J., Huss, M., Kandulski, A., Krautbauer, S., Müller, M., Liebisch, G., Buechler, C., & Tews, H. C. (2023).

Altered fecal bile acid composition in active ulcerative colitis.

Lipids in Health and Disease, 22, 199.

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Abomhya, A., Tai, W., Ayaz, S., Khan, F., Saadedeen, W., Ajala, O., & Mohamed, R. (2022).

Iron Deficiency Anemia: An Overlooked Complication of Crohn’s Disease.

Journal of Hematology, 11(2), 55.

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Abomhya, A., Tai, W., Ayaz, S., Khan, F., Saadedeen, W., Ajala, O., & Mohamed, R. (2022).

Iron Deficiency Anemia: An Overlooked Complication of Crohn’s Disease.

Journal of Hematology, 11(2), 55.

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Ellermann, M., & Arthur, J. C. (2016).

Siderophore-mediated iron acquisition and modulation of host-bacterial interactions.

Free Radical Biology & Medicine, 105, 68.

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Xie, H., Yu, S., Tang, M., Xun, Y., Shen, Q., & Wu, G. (2025).

Gut microbiota dysbiosis in inflammatory bowel disease: Interaction with intestinal barriers and microbiota-targeted treatment options.

Frontiers in Cellular and Infection Microbiology, 15, 1608025.

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Ellermann, M., & Arthur, J. C. (2016).

Siderophore-mediated iron acquisition and modulation of host-bacterial interactions.

Free Radical Biology & Medicine, 105, 68.

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SOLTANI, Z., RAFIEI, F., EBRAHIMi, A., & RAFIEI, R. (2021).

The Prevalence of Zinc Deficiency in Crohn’s Disease Patients.

MæDica, 16(1), 29.

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Liu, J. Z., Jellbauer, S., Poe, A., Ton, V., Pesciaroli, M., Kehl-Fie, T., Restrepo, N. A., Hosking, M., Edwards, R. A., Battistoni, A., Pasquali, P., Lane, T. E., Chazin, W. J., Vogl, T., Roth, J., Skaar, E. P., & Raffatellu, M. (2012).

Zinc sequestration by the neutrophil protein calprotectin enhances Salmonella growth in the inflamed gut.

Cell Host & Microbe, 11(3), 227.

Xie, H., Yu, S., Tang, M., Xun, Y., Shen, Q., & Wu, G. (2025).

Gut microbiota dysbiosis in inflammatory bowel disease: Interaction with intestinal barriers and microbiota-targeted treatment options.

Frontiers in Cellular and Infection Microbiology, 15, 1608025.

Read Review

Xie, H., Yu, S., Tang, M., Xun, Y., Shen, Q., & Wu, G. (2025).

Gut microbiota dysbiosis in inflammatory bowel disease: Interaction with intestinal barriers and microbiota-targeted treatment options.

Frontiers in Cellular and Infection Microbiology, 15, 1608025.

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Schneider, T., Caviezel, D., Ayata, C. K., Kiss, C., Niess, J. H., & Hruz, P. (2020).

The Copper/Zinc Ratio Correlates With Markers of Disease Activity in Patients With Inflammatory Bowel Disease.

Crohn's & Colitis 360, 2(1), otaa001.

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Schneider, T., Caviezel, D., Ayata, C. K., Kiss, C., Niess, J. H., & Hruz, P. (2020).

The Copper/Zinc Ratio Correlates With Markers of Disease Activity in Patients With Inflammatory Bowel Disease.

Crohn's & Colitis 360, 2(1), otaa001.

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Schneider, T., Caviezel, D., Ayata, C. K., Kiss, C., Niess, J. H., & Hruz, P. (2020).

The Copper/Zinc Ratio Correlates With Markers of Disease Activity in Patients With Inflammatory Bowel Disease.

Crohn's & Colitis 360, 2(1), otaa001.

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Culbertson, E. M., & Culotta, V. C. (2021).

Copper in infectious disease: Using both sides of the penny.

Seminars in Cell & Developmental Biology, 115, 19-26.

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Pickard, J. M., Zeng, M. Y., Caruso, R., & Núñez, G. (2017).

Gut Microbiota: Role in Pathogen Colonization, Immune Responses and Inflammatory Disease.

Immunological Reviews, 279(1), 70.

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Zackular, J. P., & Skaar, E. P. (2018).

The role of zinc and nutritional immunity in Clostridium difficile infection

Gut Microbes, 9(5), 469.

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Zackular, J. P., & Skaar, E. P. (2018).

The role of zinc and nutritional immunity in Clostridium difficile infection

Gut Microbes, 9(5), 469.

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Titécat, M., Rousseaux, C., Dubuquoy, C., Foligné, B., Rahmouni, O., Mahieux, S., Desreumaux, P., Woolston, J., Sulakvelidze, A., Wannerberger, K., & Neut, C. (2022).

Safety and Efficacy of an AIEC-targeted Bacteriophage Cocktail in a Mice Colitis Model.

Journal of Crohn's and Colitis, 16(10), 1617-1627.

Honap, S., Johnston, E., Agrawal, G., Al-Hakim, B., Hermon-Taylor, J., & Sanderson, J. (2020).

Anti-Mycobacterium paratuberculosis (MAP) therapy for Crohn’s disease: An overview and update.

Frontline Gastroenterology, 12(5), 397.

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Dulai, P. S. (2024).

The Potential Role of Hyperbaric Oxygen Therapy in Patients With Inflammatory Bowel Disease.

Gastroenterology & Hepatology, 20(12), 753.

Piotrowicz, G., Kot, J., Babicki, A., Banaszkiewicz, P., Piotrowicz, A., Rzeszutek, M., Rudnik, A., Zientara, P., Adamska-Mieruszewska, J., & Rydzewska, G. (2024).

The effects of hyperbaric treatment on perianal fistula activity in patients with Crohn’s disease.

Przegla̜d Gastroenterologiczny, 19(3), 321.

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Dulai, P. S. (2024).

The Potential Role of Hyperbaric Oxygen Therapy in Patients With Inflammatory Bowel Disease.

Gastroenterology & Hepatology, 20(12), 753.

Fanizza, J., Lusetti, F., Fasulo, E., Allocca, M., Furfaro, F., Zilli, A., Parigi, T. L., Radice, S., Peyrin-Biroulet, L., Danese, S., Fiorino, G., Fanizza, J., Lusetti, F., Fasulo, E., Allocca, M., Furfaro, F., Zilli, A., Parigi, T. L., Radice, S., . . . Fiorino, G. (2023).

The Role of IL-23 Inhibitors in Crohn’s Disease.

Journal of Clinical Medicine, 13(1).

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