Did you know?
Salmonella does not just tolerate your gut's inflammation, it exploits it: it out-competes your good bacteria for zinc using a special uptake pump that defeats the immune system's metal-starvation defense.
Salmonella is a genus of foodborne Gram-negative pathogens, led by the species Salmonella enterica. It invades host cells with type III secretion systems and thrives in the inflamed gut by defeating the host's metal-withholding defenses, a nutritional-immunity battle that is also its weak point.
Microbiome-targeted interventions (MBTIs) are validated using a dual-evidence logical framework. First, the intervention must realign the condition’s microbiome signature by increasing beneficial taxa that are consistently depleted and reducing pathogenic taxa that are consistently enriched. Second, the intervention must demonstrate measurable clinical benefit. Concordance of these effects in the same context validates the intervention as an MBTI and supports the clinical relevance of the microbiome signature.
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.
Read MoreSalmonella is a genus of Gram-negative, facultatively anaerobic, flagellated rods in the Enterobacteriaceae and one of the leading causes of foodborne illness worldwide. Nearly all human disease is caused by the single species Salmonella enterica, whose serovars range from typhoidal (Typhi, Paratyphi), which cause typhoid fever, to the many non-typhoidal serovars that cause gastroenteritis and invasive disease.[1] Invasive non-typhoidal Salmonella alone caused an estimated 535,000 cases and 77,500 deaths in 2017, hitting young children, elderly people, and people with HIV hardest.[2] On this database it appears as a differentially abundant taxon across human microbiome studies, usually a low-abundance signal rather than active infection.
What makes Salmonella distinctive is how it turns host defenses to its own advantage. It invades and survives inside host cells using two type III secretion systems, and it actually thrives in the inflamed gut, exploiting inflammation and outcompeting the resident microbiota.[1][3] Part of that edge is a metal-acquisition system that defeats the host's nutritional immunity, which is exactly the lens this database reads pathogens through.[3]
Salmonella are Gram-negative, facultatively anaerobic, non-spore-forming rods, typically motile by peritrichous flagella, in the family Enterobacteriaceae.[1] They tolerate bile and acid well enough to survive stomach passage and colonize the intestine, and are readily transmitted through contaminated food and water.[2]
Salmonella is a true pathogen rather than a commensal. Non-typhoidal serovars cause self-limiting gastroenteritis in healthy people but invasive, often bloodstream, disease with high mortality in vulnerable hosts (all-age case fatality around 14.5 percent),[2] while typhoidal serovars cause systemic typhoid fever.[1] A low-abundance differential signal in a microbiome study reflects an ecological shift or carriage, not necessarily active infection.
Salmonella's toolkit is built around invading and surviving inside host cells and winning the fight for nutrients in the inflamed gut.
| Virulence factor | Description and role |
|---|---|
| SPI-1 type III secretion system | Injects effectors that force host cells to engulf the bacterium, driving invasion of the intestinal epithelium.[1] |
| SPI-2 type III secretion system | Delivers a second set of effectors that let Salmonella survive and replicate inside a membrane-bound vacuole within host cells.[1] |
| Flagella and fimbrial adhesins | Peritrichous flagella and fimbriae mediate motility and attachment to the gut epithelium.[1] |
| Typhoid toxin and Vi antigen | Typhoidal serovars carry the typhoid toxin, which contributes to symptoms, and the Vi capsular antigen, which aids immune evasion.[1] |
| High-affinity zinc uptake (ZnuABC) | Lets Salmonella overcome host metal withholding and outgrow competing commensals in the inflamed gut.[3] |
Multidrug-resistant Salmonella, in both typhoidal and non-typhoidal serovars, is a growing problem that complicates treatment of typhoid fever and invasive disease.[1][2] Definitive treatment is susceptibility-guided; this page describes the organism's biology and its microbiome associations, not a treatment protocol.
Salmonella is a textbook case of a pathogen defeating nutritional immunity, and it does so by turning inflammation into an advantage.
| Metal / ion | Key features in Salmonella |
|---|---|
| Zinc (Zn) | The host neutrophil protein calprotectin sequesters zinc to starve microbes, but Salmonella's high-affinity ZnuABC importer overcomes this. As a result it thrives in the inflamed gut and outcompetes commensals; a ZnuABC mutant is rescued only when calprotectin is absent.[3] |
| Inflammation as opportunity | Rather than being suppressed by gut inflammation, Salmonella exploits it: inflammation shifts the metal and nutrient economy in ways the pathogen is equipped to win.[3] |
Read through the nutritional-immunity lens, the systems that give Salmonella its edge in the inflamed gut are also its openings.
| Weak point | Why it is exploitable |
|---|---|
| ZnuABC dependence | Because Salmonella relies on ZnuABC to beat calprotectin's zinc sequestration, reinforcing metal withholding or blocking that transporter attacks a system it needs to thrive.[3] |
| Colonization resistance | A healthy, intact microbiota resists Salmonella; the pathogen exploits inflammation to break that resistance, so protecting the barrier and community limits it.[3] |
| Susceptibility-guided therapy | Definitive treatment is antibiotics chosen by susceptibility, though rising resistance makes this harder.[2] |
For a pathogen, an intervention is anything that clears it or blunts its advantage. Clinical treatment is antibiotics managed by clinicians; the entries below are classified by our validation method, and this is not medical advice. The microbiome through-lines are colonization resistance and nutritional immunity.
| Intervention | Class | Status |
|---|---|---|
| Susceptibility-guided antibiotics | Drug | Validated |
| Colonization resistance (healthy microbiota) | Concept | Validation In Progress |
| Metal-withholding (zinc) support | Concept | Validation In Progress |
| Intervention | Mechanism |
| Susceptibility-guided antibiotics | Standard of care for invasive disease and typhoid, chosen by susceptibility as resistance rises.[2] |
| Colonization resistance | An intact microbiota competes with Salmonella and resists its colonization; the pathogen must break this to establish.[3] |
| Metal-withholding support | Reinforcing host zinc sequestration targets the ZnuABC system Salmonella uses to thrive in the inflamed gut.[3] |
Unnecessary disruption of the resident microbiota (for example needless broad-spectrum antibiotics), which weakens the colonization resistance that normally keeps Salmonella out.[3]
Where Salmonella (NCBI:txid590) appears as a differentially abundant taxon across the Microbiome Medicine corpus. Each row aggregates every experiment in which the organism moved in a given condition; direction is its change in the case/exposure group, and grade is the strongest single study's methodology weight (A·D·S·C·R), the same engine that grades every signature on this site.
Across 26 conditions and 29 studies, the signal is genuinely mixed: enriched in 12, depleted in 9, and direction-conflicting in 5 (directional agreement 0.57). Because Salmonella is a low-carriage pathogen rather than a stable resident, its appearances here are best read as ecological signals or carriage, not infection, so the aggregate evidence tier is Low.
How to read these. Salmonella is not a normal stable resident of the gut, so a low-abundance differential signal usually reflects transient carriage, exposure, or an ecological shift rather than active infection. Genus-level detection groups all Salmonella together and cannot resolve serovar, which matters because typhoidal and non-typhoidal serovars differ greatly. This is why direction can conflict between cohorts and the aggregate tier stays Low.
Internal summaries of the 28 studies we reviewed in which Salmonella was a differential taxon across this corpus.
This study characterized the peripheral blood microbiome of tuberculosis (TB) patients using RNA sequencing, aiming to find non-sputum biomarkers for TB diagnosis. The researchers focused on identifying Mycobacterium tuberculosis (Mtb) genome-derived small RNA molecules, specifically rRNA-derived small RNAs (rsRNAs), circulating in blood. They analyzed blood microbiome RNA signals across bacteria, fungi, archaea, and viruses, and then tested candidate Mtb rsRNAs as potential diagnostic markers. Small RNA sequencing was also performed on plasma exosomes to further probe these RNA signatures.
The initial analysis used RNA sequencing data from the blood of TB patients and healthy controls retrieved from the NCBI-SRA public database. Small RNA sequencing was additionally performed on plasma exosomes from TB patients and healthy controls. Candidate Mtb rsRNA levels were then validated by RT-qPCR in a separate cohort of 73 TB patients and 62 healthy controls. Together these groups combined public sequencing data with a defined clinical validation cohort.
The blood microbiome of TB patients contained RNA signals from bacteria, fungi, archaea, and viruses, with bacteria making up more than 97% of the total signal. TB patients showed reduced blood microbial diversity and reduced abundance of six Mycobacterium-associated bacterial genera, including Mycobacterium and Priestia. Mtb-derived rsRNAs were detectable in blood and plasma exosomes, distinguishing TB patients from healthy controls in the validation cohort of 73 patients and 62 controls.
These findings suggest that blood microbiome signatures and circulating Mtb-derived rsRNAs could serve as non-sputum, blood-based diagnostic biomarkers for tuberculosis. This approach could help address the ongoing challenge of early TB diagnosis, particularly for patients who cannot easily produce sputum samples. The reduced microbial diversity and altered Mycobacterium-associated genera also point to broader shifts in the blood microbiome accompanying active TB infection. Validating these markers in a defined patient cohort supports their potential clinical translation as a diagnostic test.
This case-control study characterized the gut microbiome in older adults with Alzheimer disease (AD) and mild cognitive impairment (MCI), comparing them to cognitively normal controls. Researchers extracted DNA from fecal samples and sequenced PCR products using Nanopore technology. They applied diversity indices, principal coordinate analysis, PERMANOVA, and LEfSe to identify microbial differences among the three groups. The study aimed to determine whether gut microbiome composition and diversity differ across the cognitive spectrum from healthy aging to dementia.
The study recruited 104 participants aged 60 years and older from urban and rural populations in Uganda. Participants were categorized into AD, MCI, and control groups based on Montreal Cognitive Assessment (MoCA) scores and ICD-11/DSM-V diagnostic criteria. This design allowed comparison of gut microbiome features across a spectrum of cognitive status within an African population, a group underrepresented in prior microbiome-dementia research.
Gut microbiome diversity, measured by the Chao1 and Shannon indices, was significantly reduced in patients with AD compared to the other groups. This reduced diversity aligns with prior findings that AD is associated with altered abundance of specific microbial taxa. The abstract text provided ends before detailing which specific taxa were enriched or depleted in the AD group, so those specifics cannot be reported here.
The findings support the idea that reduced gut microbial diversity is linked to Alzheimer disease and may reflect disruption of the gut-brain axis, including increased intestinal permeability, systemic inflammation, and oxidative stress. Because this research was conducted in Uganda, it extends microbiome-dementia evidence to an African population, broadening the generalizability of prior findings from other regions. These results reinforce the potential of gut microbiome diversity as a marker of neurodegenerative risk and support further investigation into the microbiome as a target for aging-related cognitive health interventions.
This study examined how fasting changes the gut microbial community and whether combining fasting with microbiota-accessible carbohydrates (MACs) could be used to deliberately reshape gut bacteria. The researchers tested whether fasting creates conditions that make MAC administration more effective at increasing specific commensal bacteria. They also compared fecal IgA levels between fasting plus MAC intervention and MAC administration alone. The effects of different types of MACs on the resulting microbiota composition were also assessed.
The abstract does not specify a human cohort or sample size, and the experiments appear to be conducted in an animal or laboratory model system used to test fasting and MAC interventions on the gut microbiome. No demographic, clinical, or population details are given. The subjects were evaluated for changes in gut bacterial composition and fecal IgA levels following the interventions.
Fasting altered the structure of the gut microbial community on its own, and combining fasting with MAC administration produced more profound effects than MAC administration alone. The fasting plus MAC intervention increased specific gut bacteria and raised fecal IgA levels compared with MACs given without fasting. These compositional changes were specific to the type of MAC used, and the researchers identified a protocol that effectively combined fasting with MACs to increase levels of Bifidobacterium.
The findings suggest that fasting can prepare a favorable gut environment that enhances the ability of microbiota-accessible carbohydrates to selectively modulate specific bacterial populations. This points to a practical strategy for targeted, MAC-specific enrichment of beneficial bacteria such as Bifidobacterium by pairing dietary carbohydrate interventions with fasting periods. Because the effect also raised fecal IgA, fasting plus MAC protocols may influence mucosal immune readouts alongside microbiome composition. Salmonella, Salmonella enterica, typhoid, and Enterobacteriaceae are not mentioned in this abstract.
This study examined cocoa (Theobroma cacao L.) bean fermentation, the spontaneous process that shapes the final flavour of chocolate. The researchers investigated how abiotic factors (pH and temperature) and biotic factors (bacterial and fungal microbiota) interact to produce key flavour attributes in premium chocolate. They used genome-resolved metagenomics to identify the metabolic traits within the fermentation microbial community responsible for flavour development. They then tested whether a defined microbial consortium could reproduce those fine flavour attributes under controlled conditions.
The study drew on cocoa bean fermentation samples collected from farms in Colombia. From these samples, the researchers characterized the natural bacterial and fungal community and used genome-resolved metagenomics to build a picture of the metabolic capacities present. They then assembled a separate, defined and metabolically competent microbial consortium, rather than studying a human or animal cohort, to test controlled fermentation. A trained tasting panel was also used to evaluate the resulting chocolate.
The pH, temperature, and combined bacterial and fungal microbiota composition of the fermentation samples all influenced key flavour attributes of the resulting premium chocolate. Genome-resolved metagenomics showed that the metabolic traits needed for flavour development were redundantly encoded across multiple members of the fermentation community, not confined to a single organism. Using a defined microbial consortium built from this information, the researchers replicated fine flavour attributes of chocolate under controlled conditions. This was confirmed through omics analyses, metabolic network modeling, and evaluation by a trained tasting panel.
These findings show that the flavour-relevant functions of spontaneous cocoa fermentation can be captured in a defined, reproducible microbial consortium rather than relying on uncontrolled natural fermentation. This provides a basis for designing standardized fermentation starters that can reliably reproduce fine chocolate flavour characteristics. Such starters could help cocoa producers achieve consistent premium quality across batches and locations. The approach also demonstrates a model for linking metagenomic and metabolic data to sensory outcomes in food fermentation more broadly.
This study examined the tumor-associated microbiome in colorectal cancer (CRC), comparing young-onset CRC (yoCRC, diagnosed under age 50) to average-onset CRC (aoCRC, diagnosed over age 60). Researchers used 16S rRNA amplicon sequencing on tumor tissue and paired adjacent non-malignant tissue to characterize microbial composition. They applied multiple bioinformatics tools (Phyloseq, microbiomeSeq, metagenomeSeq, and NetComi) alongside statistical tests including PERMANOVA, ANOVA, and Wilcoxon tests to assess differences in microbial diversity and community structure between the two groups.
The study included fresh frozen tumor and paired adjacent non-malignant tissue specimens prospectively collected from 136 patients with young-onset CRC and 140 patients with average-onset CRC. The yoCRC group was defined as patients diagnosed before age 50, while the aoCRC group consisted of patients diagnosed after age 60. Clinical and tumor characteristics, such as tumor location and stage, were also recorded for both cohorts.
yoCRC tumors were more often left-sided, rectal, and diagnosed at stage IV compared to aoCRC tumors. yoCRC tumors also showed significantly higher microbial alpha diversity and distinct beta diversity patterns relative to aoCRC tumors. Akkermansia and Bacteroides were enriched in yoCRC tumors, whereas aoCRC tumors showed greater relative abundances of Bacillus, Staphylococcus, Listeria, Enterococcus, Pseudomonas, Fusobacterium, and Escherichia/Shigella (the Enterobacteriaceae-associated Escherichia/Shigella group).
These findings suggest that yoCRC has a distinct intratumoral microbial profile compared to aoCRC, indicating that age of onset may be linked to different microbial dysbiosis patterns in CRC development. The clinical differences in tumor location and stage, paired with microbial differences, imply that yoCRC may represent a biologically distinct disease process rather than simply an earlier-onset version of aoCRC. This raises the possibility that microbiome-informed diagnostics or risk stratification could eventually help address the rising incidence of yoCRC.
This pilot prospective cohort study examined whether ethnicity influences gut microbiome dysbiosis in pregnancies complicated by gestational diabetes mellitus (GDM). The researchers also investigated whether diet and lifestyle modifications made after a GDM diagnosis could modulate the gut microbiome. Fecal samples were collected at two time points, 24 to 28 weeks and 36 to 40 weeks of gestation, and analyzed using targeted 16S rRNA gene-based amplicon sequencing. Statistical comparisons between groups used PERMANOVA, differential abundance testing used DeSeq2, and functional predictions were generated with PICRUSt2.
The cohort included 53 women with GDM and 16 women without GDM, all residing in Singapore. Participants belonged to three Asian ethnic groups: Chinese, Malay, and Indian. This design allowed comparison of gut dysbiosis patterns both across GDM status and across ethnic background within the same population.
Among women with GDM, gut microbiomes from the different ethnic groups shared common features rather than diverging by ethnicity. This suggests that GDM-related dysbiosis is a relatively consistent phenomenon across the Chinese, Malay, and Indian groups studied. The abstract indicates that ethnicity was not a major driver of the microbiome differences observed in these GDM pregnancies.
If GDM-associated gut dysbiosis is largely independent of Asian ethnic background, microbiome-targeted strategies for GDM may generalize across these ethnic groups rather than needing ethnicity-specific approaches. This supports the idea that dietary and lifestyle interventions after a GDM diagnosis could be evaluated and applied similarly across diverse populations. As a pilot study, these findings point to the need for larger cohorts to confirm whether microbiome-based interventions can be standardized across ethnicities.
This study examined how the gut microbiome and serum metabolome differ between people with lactose intolerance (LI) and those without it. The researchers combined a paired-sample analysis of American Gut Project (AGP) data with metagenomic and untargeted metabolomic analyses in a separate cohort. They also performed fecal microbiota transplantation (FMT) experiments to test whether the LI-associated gut microbiome could influence inflammatory outcomes. The goal was to characterize the interaction between gut microbiota and circulating metabolites in LI.
The study drew on two data sources: paired samples from the American Gut Project (AGP), a large public microbiome dataset, and a Chinese cohort in which metagenomic and metabolomic profiling was performed. The abstract does not give exact sample sizes for either group. FMT experiments were also conducted, implying an animal model component, though further details are not specified in the abstract.
Fourteen microbial genera differed significantly between LI and control individuals in the AGP data. In the Chinese cohort, a machine learning approach identified seven bacterial species and nine metabolites that could distinguish the two groups. Notably, increased Escherichia coli in the LI group was negatively correlated with several metabolites, including PC (22:6/0:0), indole, and Lyso PC, while reduced levels of Faecalibacterium prausnitzii and Eubacterium rectale were positively associated with other metabolic changes.
The findings suggest that lactose intolerance is accompanied by a distinct gut microbial and metabolic signature, not just a lactase enzyme deficiency. The rise in Escherichia coli alongside depletion of beneficial short-chain-fatty-acid producers like Faecalibacterium prausnitzii and Eubacterium rectale points to a shift toward a more pro-inflammatory microbial community. This raises the possibility that microbiome-targeted interventions could help manage LI-related gastrointestinal symptoms, and the FMT experiments support a causal link between this altered microbiome and inflammatory outcomes.
This prospective cohort pilot study investigated whether oral, vaginal, and stool microbial communities could serve as non-invasive diagnostic biomarkers for endometriosis. Researchers self-collected samples from each of the three body sites at a single time point, then performed 16S rRNA amplicon sequencing followed by bioinformatics analysis. Diversity analyses and LEfSe were used to compare microbial composition and identify differentially abundant taxa across groups.
The study enrolled sixty-four age- and sex-matched subjects recruited at Nepean Hospital and the UNSW Microbiome Research Centre in Australia. Participants were divided into three cohorts: 19 healthy controls, 24 non-endometriosis patients, and 21 patients with confirmed endometriosis. All participants other than healthy controls underwent laparoscopic surgical assessment, with histology performed on excised lesions to confirm diagnosis.
Oral microbiota composition differed significantly between the three cohorts, as did stool microbiota composition. LEfSe analysis identified differentially abundant taxa distinguishing each group. Notably, Fusobacterium was enriched in the oral samples of patients with moderate or severe disease.
These findings suggest that oral and stool microbial signatures, rather than vaginal samples alone, may carry diagnostic signal for distinguishing endometriosis from non-endometriosis and healthy states. The enrichment of Fusobacterium in more severe disease raises the possibility that microbial shifts track with disease severity. If validated in larger cohorts, this approach could support development of a non-invasive diagnostic test that reduces reliance on laparoscopic surgery for endometriosis diagnosis.
This study investigated the microbial and metabolic profile of the gut-lung axis in children with pulmonary arterial hypertension associated with congenital heart disease (PAH-CHD). The researchers used an integrated multi-omics approach, analyzing metabolites and microbiota from both the gut and lower respiratory tract. Their goal was to characterize how gut and pulmonary microbiome and metabolome profiles relate to each other in PAH-CHD and to explore the potential diagnostic value of these profiles.
The study recruited 15 healthy individuals and 15 patients with pulmonary arterial hypertension due to congenital heart disease. Participants were drawn from Fuwai Yunnan Hospital, Chinese Academy of Medical Sciences, and Kunming Children's Hospital. This design allowed direct comparison of gut and lower respiratory tract samples between affected children and healthy controls.
The gut and pulmonary microbiota of children with PAH-CHD showed an increased abundance of beneficial symbionts compared to healthy individuals. These microbial shifts were closely linked to accompanying metabolite changes, indicating coordinated alterations across the gut-lung axis. The abstract does not specify particular taxa such as Salmonella, Salmonella enterica, typhoid-associated organisms, or the Enterobacteriaceae, so no claims about those groups can be made from this study.
The findings support the idea that the gut-lung axis is disrupted in pediatric PAH-CHD and may play a role in disease progression through immune and metabolic pathways. Because distinct microbiome and metabolome signatures were identified, these profiles could potentially serve as aids in diagnosing PAH-CHD. Further validation would be needed before such profiles could be used clinically, but the results point toward the microbiome as a relevant factor in this cardiopulmonary condition.
This study used metagenomic sequencing to examine how chemotherapy affects the gut microbiota and antibiotic resistance genes (ARGs) in patients with acute leukemia (AL). Researchers compared stool samples collected before and after chemotherapy to track shifts in microbial composition and resistance gene carriage. The analysis also explored how antibiotic dosage shapes microbiota and ARG networks, and how gut microbial species relate to circulating inflammatory markers.
The subjects were patients diagnosed with acute leukemia who provided stool samples both before and after undergoing chemotherapy. The abstract does not give an exact number of patients, so the precise cohort size cannot be stated. Blood samples from these same patients were also analyzed for inflammatory biomarkers alongside the paired stool metagenomes.
Post-chemotherapy stool samples showed decreased alpha diversity and greater sample-to-sample dispersion compared with pre-chemotherapy samples, along with shifts in the abundance of specific bacterial taxa. Enterococcus, Klebsiella, and Escherichia coli were identified as the most prevalent carriers of antibiotic resistance genes. Correlation analysis linked specific microbial species to inflammatory markers, including C-reactive protein (CRP) and adenosine deaminase (ADA), and co-occurrence networks connected 179 microbial and ARG nodes across 206 edges. Treatment with cephamycin and sulfonamide antibiotics was associated with the emergence of multidrug-resistant Klebsiella colonization.
The findings suggest that chemotherapy in acute leukemia patients disrupts gut microbial balance in ways that favor colonization by resistant, potentially pathogenic Enterobacteriaceae members such as Klebsiella and E. coli. The observed links between specific antibiotics, resistant bacteria, and inflammatory biomarkers highlight the need for careful antibiotic selection and dosing during leukemia treatment to limit multidrug-resistant colonization. These data support closer monitoring of gut microbiota and ARG dynamics as a tool for anticipating infection risk and inflammatory complications in immunocompromised leukemia patients.
This study examined the bacterial tear film microbiome in aqueous-deficient dry eye, comparing Sjogren's syndrome (SS) and non-Sjogren's syndrome (NSS) dry eye to healthy eyes. Researchers sequenced the V3-V4 region of the 16S rRNA gene from tear film DNA samples using the Illumina HiSeq2500 platform. Taxa were assigned using the QIIME pipeline, and alpha and beta diversity were assessed statistically in R. Differences between groups were further characterized using principal coordinate analysis (PCoA), differential abundance testing, and network analysis.
The study included tear film samples from 33 healthy individuals, 17 individuals with Sjogren's syndrome dry eye, and 28 individuals with non-Sjogren's syndrome dry eye, for a total of 78 participants. The abstract does not provide further demographic details such as age, sex, or geographic location of the cohorts.
The phyla Actinobacteria, Firmicutes, and Bacteroidetes showed significant changes in both SS and NSS dry eye compared to healthy eyes, while Lactobacillus and Bacillus were the predominant genera across all three groups. PCoA and heat map analyses revealed that SS and NSS samples formed distinct clusters separate from the healthy cohort. Several genera, including Prevotella, Coriobacteriaceae UCG-003, Enterococcus, Streptomyces, Rhodobacter, Ezakiella, and Microbacterium, were significantly increased in the disease groups relative to healthy eyes.
These findings suggest that aqueous-deficient dry eye, whether associated with Sjogren's syndrome or not, is accompanied by a distinct shift in the ocular surface microbiome rather than a uniform or random change. The clear separation between disease and healthy clusters indicates the tear microbiome could potentially serve as a biomarker to help distinguish dry eye subtypes. This work supports further investigation into whether these microbial shifts contribute to, or result from, the inflammatory processes seen in aqueous-deficient dry eye.
This study examined the oral (saliva) microbiome composition of diverse human populations from southwestern Angola and Zimbabwe. It used the non-human sequencing reads recovered from an expanded exome capture approach, repurposing genomic data to characterize salivary bacterial communities. The aim was to add southern African, non-industrialized populations to the global picture of oral microbiome composition and diversity, which remains poorly understood on a broad scale.
The sample comprised 52 individuals drawn from eight ethnolinguistically diverse southern African populations. These included the Kuvale, Kwepe, Himba, Tjimba, Kwisi, Twa, and !Xun from Angola, and the Tshwa from Zimbabwe. The groups represented a range of subsistence strategies, including foragers, food-producers, and peripatetic communities that provide services to dominant neighboring groups.
Neisseria, Streptococcus, Prevotella, Rothia, and Porphyromonas were the five most frequent genera across all southern African groups, consistent with patterns reported in other human populations worldwide. Neither host genetics nor livelihood strategy appeared to shape the overall oral microbiome profile, pointing to a broadly homogeneous core community. However, some individuals from the Tshwa and Twa forager groups showed an enrichment of pathogenic genera belonging to the Enterobacteriaceae family, a family that includes Salmonella and other clinically relevant organisms.
The findings suggest that the human oral microbiome maintains a stable, homogeneous core composition across ethnolinguistically and subsistence-diverse populations, independent of genetic ancestry or lifestyle. This supports the idea that core oral genera are a conserved feature of human biology rather than a product of industrialization or diet alone. The localized enrichment of pathogenic Enterobacteriaceae in specific forager subgroups also highlights that certain communities may carry distinct risks worth further investigation in relation to oral and systemic health.
This study examined the uterine microbiome of post-partum dairy cows using deep shotgun metagenomic sequencing. Researchers compared microbial ecology and diversity in cows with metritis, purulent vaginal discharge, and no disease. The goal was to characterize taxonomic composition and identify differences in community structure associated with metritis.
The study drew on intrauterine swab samples from post-partum dairy cows across 24 commercial California dairy farms. A subset of 95 samples was analyzed out of a larger collection of 307 individual cow samples. Cows within 21 days post-partum were classified into three clinical groups: control (n = 32), metritis (n = 33), and purulent discharge (n = 31), based on the appearance and odor of vaginal discharge.
All three clinical groups showed highly diverse uterine microbial communities, with the top 12 most abundant genera accounting for only about 8.8 to 10.3 percent of mean relative abundance across groups. Alpha diversity was lower in samples from cows with metritis and purulent discharge compared to control cows. PERMANOVA testing showed a statistically significant difference in overall microbial community composition (beta diversity) between groups.
The findings suggest that uterine disease states in post-partum dairy cows are associated with reduced microbial diversity rather than dominance by a single pathogen, reflecting a broader ecological shift in the uterine environment. Deep shotgun sequencing offers a more complete picture of this community than earlier culture-based or amplicon-based approaches. These results could inform future work on diagnosing and managing metritis through microbiome-based markers rather than single-organism detection.
This study examined how delivery mode shapes the early gut microbiota of newborns using high-resolution shotgun sequencing. Researchers tracked the composition and dynamics of the neonatal gut microbiome over the first month of life. The design specifically compared elective cesarean section against vaginal delivery to sidestep the confounding effect of emergency cesareans, which can muddy conclusions about delivery mode's true influence.
The cohort consisted of Tunisian newborns, with stool samples collected from 5 infants born by elective cesarean section and 5 born vaginally. Samples were taken longitudinally at Day 0, Day 15, and Day 30 after birth. This is a small, delivery-mode-stratified newborn cohort rather than a large population sample.
Bacterial richness and diversity were similar between the elective cesarean and vaginally delivered groups, and both showed a shift in microbiota community composition during the first two weeks regardless of delivery mode. Both groups were dominated by Proteobacteria, Actinobacteria, and Firmicutes. However, starting from the second week, cesarean-delivered infants showed an underrepresentation of Bacteroides alongside an enrichment of opportunistic pathogenic species belonging to the ESKAPE group.
The findings suggest that even elective, non-emergency cesarean delivery is associated with a distinct early gut microbiota signature marked by Bacteroides depletion and ESKAPE pathogen enrichment, not merely overall diversity differences. This points to delivery mode as an independent driver of neonatal microbiome composition beyond confounding clinical circumstances. The emergence of opportunistic ESKAPE species by two weeks of age raises questions about potential vulnerability to opportunistic infection in cesarean-born infants that merit further, larger-scale investigation.
This study examined the gut microbiota of patients with COVID-19 pneumonia using 16S rRNA gene sequencing performed on rectal swabs. Researchers compared microbial composition and diversity between patients treated in the intensive care unit (i-COVID19), patients treated in infectious disease wards (w-COVID19), and healthy controls (CTRL). The goal was to characterize how gut microbial communities differ across varying levels of COVID-19 disease severity.
The study population consisted of patients hospitalized with COVID-19 pneumonia, divided into two groups by care setting: those admitted to the intensive care unit and those managed in infectious disease wards. These two patient groups were compared against a control group without COVID-19. The abstract does not report exact sample sizes, ages, or other demographic details for these cohorts.
Patients in the ICU showed a decrease in the Chao1 index compared to both controls and ward patients, indicating lower microbial richness in the most severely ill patients, while the Shannon index showed no significant change. At the phylum level, ward patients showed an increase in Proteobacteria compared to controls. Fusobacteria and Spirochetes were both decreased relative to controls, with Spirochetes showing the greatest decrease in ICU patients specifically.
The findings indicate that gut microbial communities shift in composition and richness according to COVID-19 disease severity, with the most pronounced changes occurring in critically ill ICU patients. These preliminary results suggest the gut microbiota may hold promising biomarkers for diagnosing COVID-19 and gauging disease severity. The authors note that validation in larger cohorts could support using microbiota profiles to help stratify patients by severity.
This study examined the nasal and oropharyngeal (NOP) microbial community using 16S rRNA gene sequencing. Researchers compared the microbiota composition and diversity across groups differing in COVID-19 status and severity. The goal was to characterize how SARS-CoV-2 infection alters the local respiratory microbiome, since no reliable markers exist to predict disease prognosis in these patients.
The cohort included 21 patients affected by COVID-19, some paucisymptomatic and others admitted to the Intensive Care Unit (ICU). They were compared against 10 controls who tested negative for COVID-19, as well as 8 patients infected with other human coronaviruses (HKU1, NL63, and OC43). All samples were drawn from nasal/oropharyngeal swabs analyzed by 16S rRNA sequencing.
Chao1 index, a measure of microbial richness, was significantly lower in ICU COVID-19 patients compared to paucisymptomatic patients. Chao1 was also decreased across ICU, paucisymptomatic, and other-coronavirus groups relative to controls. Shannon diversity index, which accounts for both richness and evenness, was significantly reduced only in ICU patients compared to controls and paucisymptomatic patients. At the phylum level, Deinococcus-Thermus was detected only in controls and was absent in SARS-CoV-2 and other-coronavirus patient groups.
The progressive loss of microbial diversity in the nasal/oropharyngeal tract, most pronounced in ICU patients, suggests that upper respiratory microbiome disruption tracks with COVID-19 severity. These findings raise the possibility that 16S rRNA-based diversity indices, such as Chao1 and Shannon, could serve as candidate biomarkers to help stratify disease severity. Further research could clarify whether restoring microbial diversity or targeting specific taxa like Deinococcus-Thermus has prognostic or therapeutic relevance in COVID-19 management.
This study investigated the composition of the gut microbiome in renal transplant recipients (RTRs) and compared it with that of healthy controls. The researchers used 16S rRNA sequencing of fecal samples to characterize microbiome composition and diversity. They then applied multivariate association with linear models (MaAsLin) to identify clinical and pharmacological determinants of the gut microbiome in RTRs, including immunosuppressive drugs and antibiotic exposure.
The study included 139 renal transplant recipients (50% male, mean age 58.3 plus or minus 12.8 years) and 105 healthy controls (57% male, mean age 59.2 plus or minus 10.6 years), all participants in the TransplantLines Biobank and Cohort Study (NCT03272841). The median time since transplantation among RTRs was 6.0 years, with a range of 1.5 to 12.5 years. Fecal samples were collected from both groups for microbiome analysis.
The gut microbiome composition of RTRs was significantly different from that of healthy controls, and RTRs had significantly lower gut microbiome diversity (p less than 0.01). Proton-pump inhibitors, mycophenolate mofetil, and estimated glomerular filtration rate (eGFR) were identified as significant determinants of the gut microbiome in RTRs (p less than 0.05). These findings point to specific medications and kidney function as key factors shaping post-transplant dysbiosis, rather than transplantation alone.
The findings indicate that renal transplant recipients experience measurable intestinal dysbiosis linked to specific modifiable factors, particularly proton-pump inhibitor use and mycophenolate mofetil therapy. This suggests that clinicians managing RTRs might consider the gut microbiome impact of routine medication choices as part of post-transplant care. Further research could explore whether adjusting these determinants influences microbiome recovery or long-term transplant outcomes.
This cross-sectional study used shotgun metagenomic sequencing of fecal samples to identify gut microbial species associated with polycystic ovary syndrome (PCOS). Researchers compared the gut microbiota composition of women with PCOS to that of women without the condition. They also collected clinical parameters, including body mass index, endocrine hormone levels, and glycemia, to test for correlations with the microbial findings.
The study included 14 reproductive-aged women diagnosed with PCOS and 14 control women, all recruited from an academic Centre for Reproductive Medicine. Fecal samples from these 28 participants underwent shotgun metagenomic sequencing. Clinical and metabolic data were gathered from the same women for correlation analysis.
Several microbial strains were significantly more abundant in the PCOS group, including Parabacteroides merdae, Bacteroides fragilis, and strains of Escherichia and Shigella, while Faecalibacterium prausnitzii was enriched in controls. Metagenomic species analysis showed that the microbial profiles of the PCOS group were negatively correlated with those of the control group. Microbial species associated with PCOS were positively correlated with endocrine disturbances, including higher body mass index and elevated serum testosterone levels.
The findings support a pathological association between gut dysbiosis and PCOS, linking specific bacterial taxa to hormonal and metabolic disturbances seen in the condition. The enrichment of Escherichia and Shigella strains alongside depletion of the beneficial species Faecalibacterium prausnitzii suggests a shift toward a more pro-inflammatory gut environment in PCOS. These results point to the gut microbiome as a potential target for understanding or managing the endocrine and metabolic features of PCOS, though further work is needed to establish causality.
This cross-sectional study examined whether the gut microbiota is associated with extraintestinal joint inflammation in patients with inflammatory bowel disease (IBD). Stool samples were collected and DNA was sequenced on the Illumina platform, with reads quality-controlled using SHI7 and processed with SHOGUN. Microbial abundance and diversity were assessed with QIIME, and compositional biomarkers distinguishing groups were identified using LEfSe. The study also evaluated microbial functional pathways, including tyrosine degradation, and examined history of bowel surgery as a possible source of variability.
One hundred eighty patients were included in the analysis, divided into four groups: those with IBD-associated arthropathy (IBD-A), IBD without arthropathy (IBD-N), rheumatoid arthritis (RA), and non-IBD, nonarthritis controls. The abstract does not give a numeric breakdown of how many patients fell into each of the four groups. This design allowed direct comparison of gut microbial composition across intestinal and joint-related inflammatory phenotypes.
IBD-A was associated with an increased abundance of microbial tyrosine degradation pathways compared with IBD-N (P = 0.02). IBD-A and RA patients both showed an increased abundance of Clostridiaceae compared with controls (P = 0.045), suggesting a shared microbial signature across two distinct arthritis-associated conditions. History of bowel surgery was also identified as a significant source of variability among IBD patients (P = 0.001) and was linked to decreased alpha diversity.
The shared enrichment of Clostridiaceae in both IBD-associated arthritis and rheumatoid arthritis suggests a common gut microbial feature may underlie joint inflammation across different autoimmune and inflammatory contexts. Altered tyrosine degradation pathways in IBD-A point to a possible metabolic mechanism linking gut microbes to extraintestinal disease manifestations. The findings also highlight bowel surgery history as an important confounder to account for in future microbiome studies of IBD patients. Together, these results support further investigation of Clostridiaceae and related microbial pathways as potential targets or biomarkers for arthritis in IBD.
This study examined whether commensal intestinal bacteria from human infants can regulate allergic responses to food. Researchers colonized germ-free mice with fecal bacteria from either healthy infants or infants with cow's milk allergy (CMA). They then compared the mice's susceptibility to anaphylactic reactions against a cow's milk allergen, along with differences in bacterial composition and ileal gene expression between the two groups.
The human component involved fecal samples from healthy infants and infants diagnosed with cow's milk allergy, used as donor material for colonization. The abstract does not give an exact number of infant donors. The bulk of the experimental work was carried out in germ-free mice colonized with these human-derived bacterial communities.
Mice colonized with bacteria from healthy infants were protected against anaphylactic responses to a cow's milk allergen, while mice colonized with bacteria from CMA infants were not. Bacterial composition clearly separated the healthy and CMA groups in both the original infant donors and the colonized mice. The two groups of colonized mice also showed distinct ileal epithelial transcriptome signatures, and correlating bacterial taxa with these gene expression changes identified the clostridial species Anaerostipes caccae as linked to protection against the allergic response.
The findings show that specific intestinal bacteria, rather than the microbiome in general, are critical for regulating allergic responses to food in early life. Identifying Anaerostipes caccae as a protective species suggests a concrete, testable target for interventions aimed at preventing or treating food allergy. This supports the broader hypothesis that early-life disruptions to gut bacterial communities, from factors such as antibiotic use, diet, Caesarean birth, or formula feeding, may contribute to the rising prevalence of food allergy.
This study examined the gut microbiota associated with colorectal adenoma (CRA) and intramucosal colorectal cancer (CRC), building on prior work linking Fusobacterium nucleatum to advanced colorectal carcinoma progression. Researchers used metagenomic analysis of the V3-V4 region of the 16S ribosomal RNA gene to profile bacterial communities from colonoscopy aspirates. The linear discriminant analysis (LDA) effect size (LEfSe) method was applied to detect microbial dysbiosis and identify taxa that differed in abundance between groups.
The study included 81 Japanese patients undergoing colonoscopy, comprising 47 patients with colorectal adenoma and 24 patients with intramucosal colorectal cancer. An additional 10 healthy subjects served as controls. All samples were derived from colonoscopy aspirates rather than stool, distinguishing the sampling approach from many other gut microbiome studies.
LEfSe analysis revealed significant differences in bacterial abundances between healthy controls and patients with CRA or intramucosal CRC. Notably, Fusobacterium varium, rather than the more commonly implicated F. nucleatum, was found to be statistically more abundant in patients with CRA and intramucosal CRC compared to healthy subjects. This suggests a specific dysbiotic signature involving F. varium is present even at these earlier stages of colorectal neoplasia.
The findings indicate that F. varium is at least partially involved in the pathogenesis of colorectal adenoma and intramucosal colorectal cancer, expanding the Fusobacterium-CRC association beyond F. nucleatum to an earlier point in disease progression. This raises the possibility that F. varium could serve as a microbial marker for early neoplastic changes in the colon. Further work would be needed to determine whether this association reflects a causal role or a marker of the changing gut environment during adenoma-to-carcinoma progression.
This study investigated dysbiosis of the gut microbiota in Parkinson's disease (PD) patients from Central Italy. The researchers used 16s ribosomal RNA gene amplicon sequencing to characterize fecal microbiota composition. They also examined dietary and lifestyle data alongside clinical variables to identify confounders and predictors that might correlate with clinical phenotypes. The aim was to find potential microbiota-based correlates of PD status and severity.
The study included 152 fecal samples collected from 80 PD patients and 72 healthy controls. Patients were enrolled according to tight inclusion criteria, though the abstract does not specify the exact nature of those criteria. Age, sex, and weight loss were treated as confounding factors in the analysis, while PD status, age, Body Mass Index, cereal consumption, weight gain, and physical activity were treated as predictors.
Fecal levels of Lactobacillaceae, Enterobacteriaceae, and Enterococcaceae were significantly higher in PD patients than in healthy controls. Lachnospiraceae, by contrast, were significantly reduced in PD patients. Lower Lachnospiraceae and higher Enterobacteriaceae levels also correlated with increased disease severity, linking this specific bacterial family shift to clinical progression.
The findings reinforce the hypothesis that gut microbiota dysbiosis is associated with Parkinson's disease, with the Enterobacteriaceae family emerging as a marker that tracks with disease severity. This suggests dysbiosis is not just present in PD but may relate to how advanced the disease is in a given patient. The results support continued investigation of specific bacterial families, particularly Enterobacteriaceae and Lachnospiraceae, as potential biomarkers or targets tied to clinical phenotype in PD.
The study examined how a single, low-concentration dose of the organophosphate insecticide trichlorfon affects the gastrointestinal microbiome of the Japanese quail. Researchers used next-generation sequencing of 16S rRNA gene amplicons to characterize bacterial communities in three sample origins: caecum, large intestine, and faeces. The design captured short-term microbial community responses following oral insecticide exposure, mimicking how birds encounter organophosphates in agricultural settings through ingestion of treated invertebrates.
The subjects were Japanese quail (Coturnix japonica), used as an avian model rather than wild birds directly. The abstract indicates both treated and untreated (control) quail of both sexes were compared, since sex-dependent differences are reported, but it does not give an exact number of birds. Sampling was drawn from three gastrointestinal compartments (caecum, large intestine, faeces) within this quail cohort.
Ingestion of the insecticide caused significant changes in gut microbiome composition and diversity between treated and untreated quail. The caecal microbiota showed sex-dependent responses that were not seen in the large intestine or faecal samples. Specifically, only treated females exhibited significant shifts in several genera within the Lachnospiraceae and Enterobacteriaceae families in the caecum.
The findings show that even a low, sublethal dose of an organophosphate insecticide can disrupt the avian gut microbiome, with effects that depend on both sex and gut region sampled. Because shifts occurred within the Enterobacteriaceae family, a group that includes Salmonella enterica and other enteric pathogens, insecticide-driven dysbiosis could plausibly alter colonization resistance against such organisms in exposed birds. This suggests pesticide exposure may have previously underappreciated indirect effects on avian gut health and disease susceptibility, warranting further study of GIT microbiota as a pathway linking agricultural chemical exposure to bird population declines.
This study examined whether early-life gut microbiota composition is associated with the natural resolution of cow's milk allergy over time. Fecal samples were profiled using 16s rRNA sequencing, with functional prediction performed via QIIME, PICRUSt, and STAMP. Children were followed longitudinally from infancy through age 8 years with clinical evaluation, milk-specific IgE levels, and milk skin prick testing.
The cohort included 226 children with milk allergy enrolled in infancy through the Consortium of Food Allergy observational study of food allergy. Fecal samples were collected at age 3 to 16 months. Participants underwent repeated clinical follow-up at enrollment, 6 months, 12 months, and yearly thereafter until age 8 years.
Milk allergy resolved by age 8 years in 128 of the 226 children, or 56.6 percent. Gut microbiome composition at age 3 to 6 months was significantly associated with milk allergy resolution by age 8 years. Children whose milk allergy later resolved showed enrichment of Clostridia and Firmicutes in their infant gut microbiome, and metagenome functional prediction supported a link between this early microbial composition and allergy outcome.
The findings suggest that specific early-life gut microbiota, particularly Clostridia and Firmicutes enrichment, may promote or mark the developmental path toward outgrowing cow's milk allergy. This raises the possibility of using early infant microbiome composition as a biomarker to predict which children are more likely to resolve their milk allergy. It also points toward gut microbiota as a potential target for interventions aimed at promoting tolerance to cow's milk.
This study used pyrosequencing to analyze the intestinal microflora of healthy Thai vegetarians and non-vegetarians. The researchers identified 893 operational taxonomic units (OTUs) covering 189 species. They compared the core gut microbiota composition between the two dietary groups and examined correlations between personal characteristics, consumption behavior, and microbial groups.
The subjects were healthy Thai adults divided into two dietary groups: vegetarians and non-vegetarians. The abstract does not give an exact number of participants, so a precise sample size cannot be stated. The comparison was structured around diet type as the key distinguishing variable between the two cohorts.
Prevotella copri was the strongest species indicator of vegetarians, present at 16.9% relative abundance, while Bacteroides vulgatus and bacteria related to Escherichia hermanii were the strongest indicators of non-vegetarians, at 4.5 to 4.7% relative abundance. The vegetarian group's core gut microbiota consisted of 11 species, compared to 20 species in the non-vegetarian group, spanning Actinobacteria, Firmicutes, and Proteobacteria common to both. Faecalibacterium prausnitzii and Gemmiger formicilis were present in 100% of subjects in both groups, while Clostridium nexile, Eubacterium eligens, and P. copri were common in most vegetarians, and non-vegetarians showed greater diversity including various Escherichia, Bacteroides, and Parabacteroides species. Age in non-vegetarians correlated strongly with Bacteroides uniformis abundance (coefficient 0.54, p = 0.001) and moderately with Alistipes finegoldii.
The findings suggest that a vegetarian diet is associated with a more Prevotella-dominant, less diverse core microbiota, while a non-vegetarian diet supports a broader core community that includes multiple Escherichia species. Because Escherichia and related Enterobacteriaceae are implicated in opportunistic and pathogenic risk, their greater representation and diversity in non-vegetarians may carry implications for gut pathogen risk. This work supports the idea that habitual diet shapes both the composition and the potential pathogen-associated risk profile of the human gut microbiome.
This study examined whether fecal microbiota composition differs between people with colorectal adenoma (CRA), a precancerous lesion, and those with normal colonoscopy findings. Researchers used Illumina sequencing of 16S rRNA genes amplified from DNA extracted from self-collected fecal samples preserved in RNAlater. They compared phylum-level community composition and abundance patterns between groups using regression, permutation testing, and random forest classification with leave-one-out validation. The goal was to determine if microbiota profiling could help identify CRA in a population-based screening context.
The study population was fecal immunochemical test-positive (FIT+) individuals undergoing colonoscopy as part of a population-based colorectal cancer screening program. Of 95 FIT+ participants, 61 had both successful fecal microbiota profiling and colonoscopy data available for analysis. Colonoscopy findings classified these participants into 24 completely normal patients, 20 with colorectal adenoma, 2 with colorectal cancer, and 15 with other conditions.
Phylum-level fecal community composition differed significantly between CRA and normal patients (permutation P = 0.02), and rank phylum-level abundance distinguished the two groups with an area under the curve of 0.767 (permutation P = 0.006). CRA prevalence was 59 percent in phylum-level cluster B versus 20 percent in cluster A (exact P = 0.01). Most of this difference reflected a three-fold higher median relative abundance of Proteobacteria taxa in CRA patients (Wilcoxon signed-rank P = 0.03, positive predictive value = 67 percent).
These findings suggest that fecal microbiota profiling, particularly elevated Proteobacteria abundance, could serve as a complementary or adjunct marker for detecting colorectal adenoma in FIT-positive screening populations. Because current fecal heme testing has limited sensitivity for CRA and colonoscopy participation is low, a microbiota-based approach could help improve early, curable-stage detection. Further validation in larger cohorts would be needed to confirm whether phylum-level clustering or Proteobacteria abundance can be translated into a practical screening tool.
This study examined the early development of the gut microbiome in young children carrying high genetic risk for type 1 diabetes (T1D). Researchers used high throughput 16S rRNA gene sequencing on monthly stool samples collected from 4 to 6 months of age until 2.2 years of age. The goal was to identify compositional changes in the gut microbiome that occur before children develop T1D related autoimmunity. Both low abundance taxa and highly abundant groups, including two closely related Bacteroides species, were assessed for their relationship to later seroconversion.
The cohort consisted of 76 children at high genetic risk for T1D, all born in the same hospital in Turku, Finland. Of these children, 29 later seroconverted to T1D related autoimmunity, and 22 of those went on to develop T1D, forming the case group. The remaining 47 children stayed healthy throughout the study period and served as controls.
Several low abundance bacterial species showed significant compositional differences between children who later seroconverted and those who remained healthy. Notably, a highly abundant group made up of two closely related species, Bacteroides dorei and a related Bacteroides species, stood out as dominant in the gut microbiome prior to the onset of autoimmunity. This finding points to an early, high abundance microbial signal associated with the path toward T1D related autoimmunity, distinct from the more subtle low abundance differences.
The early presence and dominance of Bacteroides dorei before autoimmune seroconversion suggests the gut microbiome may play an active role in the processes leading to T1D in genetically susceptible children. Because the sampling began in infancy and continued monthly, these findings support the idea that microbiome monitoring during early childhood could help identify children at elevated risk before clinical autoimmunity appears. This work adds to the broader case that environmental factors, particularly the developing gut microbiome, interact with genetic predisposition to influence autoimmune disease risk. The Salmonella and Enterobacteriaceae groups were not mentioned in this abstract, so no claims are made about them here.
This study examined how diet shapes gut microbial composition by comparing the fecal microbiota of children eating different diets. Researchers used high-throughput 16S rDNA sequencing together with biochemical analyses to characterize bacterial community composition and short-chain fatty acid output. The design set a fiber-rich, agrarian-style diet against a modern European diet to test whether microbiota differ along with dietary pattern.
The study compared fecal samples from European children (EU) with those from children living in a rural African village in Burkina Faso (BF). The BF children's diet was high in fiber content and described as similar to the diet of early human settlements around the birth of agriculture. Exact sample sizes are not given in the abstract, but the comparison was structured as two defined pediatric cohorts, one European and one rural Burkinabe.
BF children showed significant enrichment in Bacteroidetes and depletion in Firmicutes compared to EU children (P < 0.001). BF children also had a unique abundance of Prevotella and Xylanibacter, genera known to carry genes for cellulose and xylan hydrolysis, which were completely absent in EU children. BF children produced significantly more short-chain fatty acids than EU children (P < 0.001). Enterobacteriaceae, specifically Shigella and Escherichia, were significantly underrepresented in BF children relative to EU children (P < 0.05).
The findings support the idea that gut microbiota coevolved with a polysaccharide-rich diet, helping BF children extract more energy from fiber through bacterial fermentation to short-chain fatty acids. The reduced abundance of Enterobacteriaceae, including Shigella and Escherichia, in the high-fiber BF group suggests diet may also influence the balance between beneficial fiber-degrading bacteria and potentially pathogenic Enterobacteriaceae. Together these results indicate that dietary pattern is a major driver of gut microbial ecology in children, with possible downstream effects on metabolic energy harvest and gut colonization resistance.
2026-07-04
Salmonella majorTaxon page created: biology (morphology, pathogenicity, type III secretion virulence, antibiotic resistance), the zinc / nutritional-immunity metallome and vulnerabilities, interventions, the data-derived Conditions table across 26 conditions, and the full research feed.
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