Divine Aleru, Microbiome Signatures Research Coordinator

This review explores the pathophysiology, prevalence, and treatment strategies for extraintestinal manifestations (EIMs) in Crohn’s disease and ulcerative colitis, emphasizing the role of immune responses, microbiome alterations, and biologic therapies in managing these systemic conditions.

This study examines the clinical features, risk factors, and treatment outcomes of intra-abdominal abscesses (IA) and intestinal free-wall perforations (IP) in Korean patients with Crohn’s disease, highlighting the role of intestinal stricture and disease behavior in complication development.

This review explores the pathophysiology, risk factors, and management of intestinal strictures in Crohn’s Disease, emphasizing genetic, environmental, and imaging factors, as well as current therapeutic approaches.

This review explores environmental risk factors for Crohn’s disease and ulcerative colitis, highlighting modifiable exposures such as smoking, diet, and early-life antibiotic use, and their impact on disease prevention.

This review explores the role of epithelial barrier dysfunction and microbial dysbiosis in the pathogenesis of Crohn’s disease, highlighting the impact of genetic, environmental, and microbiota factors on disease progression and the potential for therapeutic strategies to restore barrier integrity and balance microbial communities.

This review focuses on the complex pathogenesis of Crohn’s Disease, exploring the roles of microbiome dysbiosis, immune system dysregulation, and environmental factors in disease progression, while highlighting novel therapeutic and diagnostic strategies

This review explores the evolving role of microbiome-targeted therapies in Crohn’s disease, focusing on microbial dysbiosis and its implications for disease progression and treatment.

The study examines the role of microbiome in IBD, highlighting its potential in diagnosing, predicting disease progression, and personalizing treatments.

This study shows that Escherichia coli Nissle exerts strong dose dependent amebicidal activity against Entamoeba histolytica through oxidative stress and structural damage, highlighting its therapeutic potential.

Escherichia coli Nissle 1917 inhibited Candida albicans growth, reduced virulence traits and protected intestinal cells, showing strong preventive potential through contact based and soluble antifungal mechanisms.

This study shows that Klebsiella pneumoniae L fucose metabolism enhances gut colonization, strengthens biofilm and adherence traits, and increases virulence signalling, identifying a functional metabolic signature relevant to microbiome based clinical risk.

This study shows that the immuno modulatory effect of Escherichia coli Nissle 1917 primes polarized colonic cells, reduces Campylobacter jejuni adhesion and survival, and rebalances NF kappa B, MAPK and Akt signaling to limit inflammation and epithelial injury.

This study shows how Escherichia coli Nissle 1917 inhibitory mechanisms act through adhesion and suppression of EPEC virulence, defining a strong microbiome signature of pathogen interference.

This study shows that Escherichia coli Nissle 1917 microcin MccM is the key factor driving EcN’s inhibition of Salmonella, improving pathogen suppression, reducing cell invasion, and lowering inflammatory cytokine responses.

This study shows that DegP secretion drives probiotic Escherichia coli DegP biofilm inhibition by repressing pathogenic biofilms through a targeted extracellular mechanism that shapes microbial competition.

This study shows how F1C fimbriae in Escherichia coli Nissle 1917 drive biofilm formation, epithelial adhesion, and intestinal persistence, defining a functional microbiome signature for stable colonization.

This review explains how adhesive threads of extraintestinal pathogenic Escherichia coli shape gut colonization, tissue tropism and invasive disease and shows how detailed adhesin profiles can inform microbiome based risk assessment and vaccine design.

E. coli Nissle 1917 demonstrates significant antibiofilm activity against P. aeruginosa, inhibiting biofilm formation and dispersing mature biofilms. Its CFS also downregulates key virulence factors and offers protection in a Galleria mellonella model.

This review shows how Salmonella reshapes the gut environment and engages in Salmonella gut infection antagonistic interbacterial interactions with commensals, and it explains how bacteriocins and type six secretion systems shape microbiome signatures and infection risk.

his review shows how siderophore microcins in Escherichia coli support competitive gut colonization, connect the fecal reservoir with urinary tract infection, and define functional microbiome signatures that combine B2 background with microcin, salmochelin and colibactin islands.

This review explains intestinal effect of Escherichia coli Nissle 1917 and its vesicles on the gut barrier, dysbiosis and mucosal immunity, and it links these microbial actions to clinical outcomes in inflammatory bowel disease and acute diarrhoea.

Escherichia coli Nissle 1917 (EcN) is a highly regarded probiotic strain with significant clinical value due to its ability to outcompete a wide range of pathogenic microorganisms in the gastrointestinal tract. Through the formation of robust biofilms on intestinal epithelial surfaces, EcN effectively blocks the adhesion and colonization of pathogens such as Salmonella, Shigella, and Klebsiella pneumoniae.

Oral delivery of a glypican-1–flagellin fusion by engineered EcN triggered systemic IgG and regulatory IL-10 in mice, confirming a safe probiotic cancer-vaccine chassis but indicating the need for stronger cellular adjuvanticity for PDAC.

What was studied?Engineered Escherichia coli Nissle 1917 Pseudomonas aeruginosa control was tested as a live targeted therapy for gut infection. The authors rebuilt the earlier “sense-and-kill” circuit in a clinically used EcN background. The circuit sensed the P. aeruginosa quorum signal 3OC12-HSL. It then triggered lysis and release of pyocin S5, an antipseudomonal bacteriocin. It […]

Engineered EcN for phenylketonuria was upgraded to SYNB1934 using biosensor-enabled PAL evolution, doubling gut phenylalanine conversion and keeping biocontainment, supporting development of an oral strain for diet-refractory PKU.

Engineered Escherichia coli Nissle 1917 for hyperammonemia (SYNB1020) safely consumed gut ammonia, improved survival in mice, and showed dose-linked metabolic activity and clearance in healthy adults, supporting clinical development for urea cycle and liver-related hyperammonemia.

Engineering Escherichia coli Nissle 1917 therapeutics enables targeted antimicrobial, mucosal, metabolic, and anticancer actions but requires parallel engineering for biosafety and colibactin control.

Escherichia coli Nissle 1917, a probiotic strain, offers significant health benefits, but its genotoxic potential due to colibactin production raises safety concerns, particularly in relation to colorectal cancer. The review underscores the need for further research on the balance between benefits and risks.

Escherichia coli Nissle 1917 reduces the incidence of acute respiratory infections in late preterm newborns during the first month of life, with no adverse effects, highlighting its potential as a prophylactic intervention in this vulnerable population.

This study demonstrates that engineered E. coli Nissle 1917 can selectively colonize colorectal adenomas and reduce tumor burden in mice. The probiotic also shows promise for non-invasive detection and treatment of CRC in humans, suggesting a novel therapeutic and diagnostic platform.

Escherichia coli Nissle 1917 (EcN) shows promise as a tumour-targeting probiotic bacterium for cancer treatment and detection. This review investigates its tumour-homing abilities and outlines future research directions to optimize its use in clinical oncology.

This review analyzes the advancements in preventing urinary catheter-related infections (CAUTIs) through scientific publications and patents, highlighting innovations like antimicrobial-coated catheters and biofilm-resistant materials, with implications for clinical practice and healthcare systems.

Probiotic Escherichia coli Nissle 1917 iron competition reduced Salmonella in inflamed murine gut by using lipocalin-2–resistant siderophores and by dampening mucosal inflammation, showing a nutritional immunity route for probiotic therapy.

Escherichia coli Nissle 1917 acute diarrhoea therapy in infants and toddlers shortened illness from 4.8 to 2.5 days, raised response to 94.5%, and was as safe as placebo.

Escherichia coli Nissle 1917 improved IBS modestly overall but clearly in postinfectious or postantibiotic IBS, was as safe as placebo, and fits a dysbiosis-linked microbiome signature that needs 10–12 weeks of therapy to show.

Escherichia coli Nissle 1917 (EcN) significantly enhances protection against human rotavirus in gnotobiotic pigs by modulating plasmacytoid dendritic cells and NK cell responses, suggesting its potential as an effective probiotic treatment for viral gastroenteritis.

Escherichia coli Nissle 1917 (EcN) is a safe and effective probiotic for maintaining remission in ulcerative colitis patients, with clinical trial evidence showing equivalence to mesalazine in relapse prevention. Its mechanisms include immune modulation, antimicrobial activity, and gut barrier reinforcement.

Escherichia coli Nissle 1917 (EcN) interferes with the invasion of human intestinal epithelial cells by various pathogens through a secreted component, not by microcins or physical contact, suggesting its potential as a therapeutic probiotic to prevent gastrointestinal infections.

This study uncovers the dual role of Escherichia coli Nissle 1917, where its beneficial antibacterial activity is linked to the ClbP protein, while its genotoxic effects are dependent on colibactin. Engineering strains that decouple these activities could lead to safer probiotic therapies.

The study explores how Escherichia coli Nissle 1917’s microcins mediate competition in the inflamed gut, showing potential for therapeutic use in enterobacterial infections and colitis management.

E. coli Nissle uses yersiniabactin to bind zinc, overcome calprotectin, and colonize the inflamed gut, defining a metal-driven microbiome signature linked to Enterobacteriaceae dominance in colitis, with clear dependence on inflammation and pH.

Probiotic-e-coli-nissle-1917 shows benefit in ulcerative colitis, infant diarrhea, and innate immune priming, with transient engraftment and microcin-based pathogen suppression, but no effect in Crohn’s disease. Safety is strong, though neonatal products require caution.

E. coli Nissle 1917 is a non-pathogenic probiotic strain that inhibits pathogenic bacteria, reduces inflammation, and strengthens intestinal barrier function, with proven clinical efficacy in treating gastrointestinal diseases.

Escherichia coli Nissle 1917 (EcN) is a rare, non-pathogenic strain of E. coli discovered during World War I from a soldier who did not get dysentery while others did. Unlike harmful E. coli, EcN acts as a probiotic: it settles in the gut, competes with bad bacteria for food and space, produces natural antimicrobials, and even helps strengthen the gut barrier.

This study evaluates the inhibitory effects of Escherichia coli Nissle 1917 (EcN) on Clostridium perfringens type A, focusing on growth inhibition, toxin production, biofilm formation, and inflammatory cytokine responses in vitro.

Escherichia coli Nissle 1917 (EcN), a probiotic with a rich history, is now being engineered for therapeutic uses beyond gastrointestinal health, including metabolic disease treatment and immune modulation. Its potential in microbiome research and live vaccine development is also being explored.

The study discusses dietary strategies to counteract the toxicity of cadmium and lead exposure, emphasizing the role of essential metals, vitamins, probiotics, and edible plants. These strategies offer a safer, more accessible alternative to traditional chelation therapy.

The study emphasizes the potential benefits of zinc and multi-mineral supplementation in reducing cadmium toxicity. It links cadmium exposure to various health issues and suggests supplementation as a strategy to mitigate its harmful effects.

The review examines how cadmium exposure affects gut microbiota, leading to dysbiosis, increased gut permeability, and systemic inflammation. It also explores the potential of probiotics to mitigate cadmium-induced toxicity, suggesting new therapeutic strategies.

This study shows that cadmium exposure disrupts gut function in zebrafish, affecting villi morphology, goblet cell mucus production, and glycoprotein distribution. These changes may impair gut defense and highlight the environmental risks of cadmium contamination.

This study highlights the use of cadmium levels in saliva and urine as indicators of smoking addiction. It shows that cadmium concentrations correlate with tobacco use, offering a non-invasive method for assessing exposure in smokers and second-hand smokers.

The review shows that urinary cadmium biomarker long-term exposure provides a stable signal of cumulative dose. Smoking, age, sex, iron status, and kidney function shape values. Proper dilution adjustment and stratification improve validity for clinical and microbiome research.

This study examines how the combination of cadmium and iron oxide nanoparticles enhances the conjugative transfer of antibiotic resistance genes in microbial communities. It emphasizes the risk of accelerated antibiotic resistance spread, especially in human pathogens, under environmental pollution.

The study explores how cadmium and copper contamination in rhizosphere soil affects the distribution of antibiotic resistance genes. It shows that these metals contribute to the spread of resistance genes through co-selection, with significant implications for environmental and public health.

The review examines the sources, accumulation, and health effects of cadmium, emphasizing its long-term toxicity, particularly its role in lung, kidney, bone, and neurological diseases. It underscores the need for continued monitoring and preventive measures for populations at risk.

This study highlights the protective effects of Lactobacillus plantarum CCFM8610 probiotics against cadmium toxicity by preserving intestinal barrier function and reducing oxidative stress, offering a potential therapeutic strategy for preventing heavy metal absorption.

The study examines how cadmium exposure alters the microbiota in rats, causing microbial translocation and metabolic shifts. The findings highlight potential biomarkers for assessing cadmium toxicity.

This study reveals how low-dose cadmium exposure disrupts gut microbiota, increasing intestinal permeability and liver injury in mice. The findings emphasize the role of microbiota in modulating toxin absorption and liver function.

This study highlights the significant impact of environmental pollutants on the gut microbiome, selecting for microbial functions that degrade xenobiotics and potentially promoting antibiotic resistance. Understanding these changes can provide insights into the role of the microbiome in detoxifying pollutants and influencing human health.

This review discusses the strategies for translating microbiome-based therapies into clinical practice for FGIDs, particularly IBS. It highlights the need for a systems approach integrating multi-omics data and patient stratification.

The study investigates how soft metals like silver, mercury, cadmium, and zinc damage bacterial dehydratases by targeting their [4Fe-4S] clusters, revealing insights into the molecular mechanisms of metal toxicity in E. coli. The findings highlight the potential for oxidative stress and inform strategies for antimicrobial resistance.

This study examines the effects of cadmium exposure on the microbiome, showing how it alters gut and blood microbiota, impacts metabolites, and links to inflammatory responses. The research reveals significant microbial shifts and potential biomarkers for Cd-induced toxicity.

Microbial metallophores are vital in sustainable agriculture, enhancing nutrient availability, promoting plant growth, and mitigating heavy metal toxicity. The study highlights their potential in bioremediation and as biocontrol agents.

The study explores the multifaceted role of bacterial siderophores in microbial community dynamics and host interactions. It highlights their impact on bacterial competition, survival, and virulence, offering insights into potential therapeutic strategies for managing infections and manipulating microbial communities.

This study shows that cadmium acts as a zinc mimetic by binding to and activating the HIZR-1 nuclear receptor, leading to the activation of high zinc homeostasis genes in C. elegans. The research highlights the overlap between cadmium and zinc responses, shedding light on cadmium’s transcriptional control mechanisms.

This study explored the role of metallothionein in cadmium toxicity, focusing on its protective and transport roles, particularly in the kidneys. It emphasizes the potential of MT-related biomarkers for assessing cadmium exposure risks in humans.

This study explored how the CzcRS3 two-component system regulates cadmium resistance in P. putida by controlling efflux pump gene expression. The findings emphasize the role of CadR in regulating this system and offer insights into potential bioremediation strategies.

This study investigates the role of ZntA in zinc and cadmium homeostasis, oxidative stress resistance, and virulence in Vibrio parahaemolyticus. ZntA protects against metal toxicity and promotes bacterial survival under stressful conditions, highlighting its importance in bacterial pathogenesis.

This study identifies CadC as a key transcriptional regulator of the cadmium resistance operon in S. aureus plasmid pI258, revealing its role in controlling cadA expression in response to metal ions like cadmium, bismuth, and lead.

The study identifies and characterizes the cadmium resistance operon in S. aureus ATCC12600. It reveals that the cadC gene is crucial for cadmium efflux and resistance but does not function as a repressor, offering new insights into cadmium resistance mechanisms.

This study explores how cadmium binds to human serum transferrin, albumin, and citrate, revealing key insights into cadmium transport and bioavailability in the bloodstream. It also highlights the potential clinical implications for understanding cadmium toxicity and therapeutic interventions.

This study investigates how albumin influences cadmium uptake in primary rat hepatocytes, revealing its protective role in reducing toxicity. The findings suggest albumin’s involvement in cadmium bioavailability and provide insights for developing therapeutic strategies to mitigate cadmium-related health risks.

The review examines the complex role of hydrogen sulfide in modulating the gut microbiome, highlighting its potential as a therapeutic agent to stabilize microbiota biofilms and reduce inflammation in diseases like IBD.

The study explored how gut microbes and chelating agents influence the bioavailability of arsenic, cadmium, lead, and mercury by assessing their intestinal permeability using a Caco-2 cell model. It found that both microbes and chelating agents reduce the permeability of these metals, mitigating their toxicity.

This study explores how altering gastric pH with omeprazole and cimetidine affects cadmium absorption from the diet and its accumulation in murine tissues, showing limited impact on tissue cadmium levels despite changes in gastric pH.

This review explores the toxic effects of cadmium exposure on multiple organ systems and its link to various diseases, including cancer and kidney dysfunction. It also discusses treatment options, including chelation therapy and nanoparticle-based interventions.

This study explores how cadmium disrupts the immune function of macrophages by inhibiting the NF-κB signaling pathway, impairing the response to LPS, and potentially contributing to immune dysfunction in diseases like COPD.

Cadmium exposure inhibits macrophage immune function through suppression of the NF-κB pathway, impairing the response to LPS. This may contribute to immune dysfunction and increased susceptibility to infections, especially in COPD patients.

The study demonstrates how cadmium exposure enhances antibiotic resistance in Salmonella enterica serovar Typhi by altering bacterial growth, biofilm formation, and antibiotic susceptibility. The findings highlight the environmental impact of cadmium in promoting resistance.

This review highlights how heavy metals alter the gut microbiota and discusses the potential of probiotics to mitigate these effects. It also emphasizes the role of advanced biosensors in detecting heavy metals in urine, supporting real-time monitoring of detoxification processes.

The study investigates how cadmium exposure alters gut and blood microbiomes in rats, linking these changes to metabolic disruptions and systemic inflammation.

This study reveals how cadmium and arsenic exposure via the food chain disrupts oxidative enzyme activity in rats, leading to significant health risks, particularly in the liver and kidneys.

The study uncovers how cadmium disrupts transition metal homeostasis in Streptococcus pneumoniae, affecting manganese and zinc uptake and contributing to oxidative stress.

Cadmium (Cd) is a highly toxic heavy metal commonly found in industrial, agricultural, and environmental settings. Exposure to cadmium can occur through contaminated water, food, soil, and air, and it has been linked to a variety of health issues, including kidney damage, osteoporosis, and cancer. In agriculture, cadmium is often present in phosphate fertilizers and can accumulate in plants, entering the food chain. Its toxicity to living organisms makes cadmium a subject of regulatory concern worldwide, particularly in industrial waste disposal and environmental monitoring.

Fecal microbiota transplantation (FMT) has demonstrated high success in treating recurrent Clostridium difficile infection, with potential benefits for other gastrointestinal disorders, including IBD, obesity, and metabolic syndrome. FMT restores microbial diversity,

This review explores the role of chelation therapy in treating arsenic and mercury poisoning, focusing on the efficacy of BAL, DMPS, and DMSA in acute cases and the challenges posed by chronic exposure. It discusses therapeutic benefits, limitations, and the need for further research.

This review explores the protective effects of selenium against arsenic and cadmium toxicity, emphasizing its role in reducing oxidative stress, inflammation, and cellular damage. The findings suggest selenium supplementation may help mitigate the harmful effects of these metals on human health.

This study explores the effects of chronic arsenic exposure on the gut microbiota and bile acid metabolism in mice, revealing significant changes in microbial composition and bile acid homeostasis, which may contribute to metabolic dysfunction and related diseases.

The study explored the impact of arsenic exposure on red blood cell parameters in rural Bangladesh, identifying sex-specific effects and changes in MCV and MCH, which may contribute to anemia or macrocytosis.

The study explored the impact of arsenic exposure on the gut microbiome and host metabolism. The results demonstrated significant changes in microbial composition, which were linked to alterations in metabolic pathways, particularly nitrogen metabolism, shedding light on arsenic’s role in disease promotion.

This study explores the sex-specific effects of chronic arsenic exposure on stromal cells and signaling in the small intestine, highlighting how arsenic disrupts trophocytes and telocytes, which regulate stem cell functions.

The study assessed arsenic exposure in Shanyin County residents through saliva and urine samples. It confirmed that saliva is a potential biomarker for total arsenic exposure, although less effective for understanding arsenic metabolism.

What was studied?This study focused on evaluating arsenic exposure through diet by assessing stool samples in populations from West Bengal, India. Given that arsenic exposure via drinking water is well-documented, the researchers aimed to explore whether stool could serve as a reliable biomarker for arsenic exposure through the food chain, particularly in areas where groundwater […]

The study examines biomarkers of inorganic arsenic exposure in humans, focusing on the metabolism and toxicological effects of arsenic. Key findings include the importance of urinary arsenic measurements and the impact of genetic differences in arsenic metabolism.

The study demonstrates how IL-10 gene knockout mice show significant changes in their gut microbiome and arsenic metabolism. These alterations contribute to higher levels of toxic arsenic metabolites, highlighting the role of host genetics in shaping exposure outcomes.

Arsenic exposure perturbs the gut microbiome in mice and rewires fecal, urinary, and plasma metabolites, including sharp shifts in indole and bile acid pathways, alongside loss of several Firmicutes families and a rise in a Clostridiales group, before any histologic injury appears.

At 100 ppb, arsenic reshaped mouse gut communities, lowered SCFA gene capacity, increased LPS and stress pathways, and enriched multidrug and conjugation genes while shifting taxa toward Akkermansia and Bifidobacterium and away from SCFA-producing Firmicutes.

In rural China, drinking water often exceeded standards, and hair arsenic was higher in exposed residents. Age, male sex, and wheat-based diet increased levels, making hair arsenic a useful long-term marker for clinical screening and for stratifying microbiome studies.

This study highlights the health effects of chronic arsenic exposure through drinking water, linking it to cancers, cardiovascular diseases, and diabetes. It emphasizes the need for monitoring arsenic levels and improving public health interventions.

This study assessed acute and chronic arsenic exposure in an Ethiopian population, finding significant health risks associated with contaminated groundwater and cigarette smoking. Biomarkers like urine and nail arsenic levels were key in understanding exposure.