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Prevotella histicola is being turned into a medicine. A single, non-colonizing strain (EDP1815) is swallowed to calm inflammation throughout the body without changing the rest of your gut bacteria.
Prevotella histicola is an immunomodulatory human commensal and a leading example of a medicine made from a microbe. It calms autoimmune inflammation, suppressing a multiple sclerosis model as effectively as interferon-beta and showing anti-inflammatory effects in early psoriasis and atopic dermatitis trials as the single-strain therapeutic EDP1815. Unlike its pro-inflammatory relative Prevotella copri, P. histicola is anti-inflammatory.
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 MorePrevotella histicola is a Gram-negative, anaerobic human commensal of the Bacteroidota, found on mucosal surfaces of the mouth and gut. It stands out on this database not as a pathogen but as an immunomodulatory, anti-inflammatory microbe: a human gut-derived strain suppresses autoimmune disease in animal models, and it is the organism behind one of the first single-strain microbial medicines.[1][2] On this database it appears as a differentially abundant taxon across many human microbiome studies.
Importantly, Prevotella is a heterogeneous genus: while Prevotella copri is linked to pro-inflammatory arthritis, P. histicola is anti-inflammatory and disease-suppressing, so the species matters.[3] A single, non-colonizing strain of P. histicola, developed as EDP1815, is swallowed to calm inflammation throughout the body without entering the bloodstream or changing the resident gut microbiota.[2] As an immunomodulatory commensal it sits outside the bacterial metallome framework this database applies to nickel- and manganese-driven pathogens; its relevance is immunological, and its presence marks an anti-inflammatory gut.
P. histicola is a Gram-negative, non-motile, strictly anaerobic rod of the Prevotella genus, a mucosa-associated commensal originally characterized from the human oral cavity and also found in the gut.[1] Its importance comes from how it engages the immune system rather than from any structural virulence trait.
P. histicola is a beneficial, immune-regulating commensal. In a preclinical model of multiple sclerosis (experimental autoimmune encephalomyelitis), it suppressed disease as effectively as interferon-beta, a standard multiple sclerosis drug, by expanding regulatory T cells in gut-associated lymphoid tissue and reducing inflammatory T cells and glial activation in the central nervous system.[1] It also suppressed the development of arthritis in humanized mice, in contrast to the pro-inflammatory role of P. copri.[3]
Its useful features are immunological, and they act from within the gut.
| Factor | Description and role |
|---|---|
| Regulatory T cell induction | Expands CD4+FoxP3+ regulatory T cells in gut-associated lymphoid tissue, tipping the immune balance toward tolerance.[1] |
| Suppression of inflammatory T cells | Lowers IFN-gamma and IL-17 producing T cells and dampens Th1, Th2, and Th17 inflammation.[1][2] |
| Gut-restricted, non-colonizing action | Acts locally in the gut without colonizing or entering the bloodstream, signaling to the immune system to reduce inflammation body-wide.[2] |
| Reduced CNS and tissue inflammation | In the multiple sclerosis model it reduced microglial and astrocyte activation and demyelinating pathology.[1] |
P. histicola is a mucosa-associated anaerobic commensal, not a metal scavenger. Its role in this database is immunological: a species whose presence is associated with an anti-inflammatory, tolerant gut, and whose depletion tracks with autoimmune disease.[4] Because the Prevotella genus contains both pro- and anti-inflammatory members, species-level identity, not just the genus, determines the direction of effect.[3]
P. histicola's associations are consistently on the anti-inflammatory, protective side.
| Association | Direction and interpretation |
|---|---|
| Multiple sclerosis | Prevotella is reduced in people with multiple sclerosis and rises with disease-modifying therapy; P. histicola suppresses the multiple sclerosis model, motivating its study as a microbial monotherapy.[4][1] |
| Rheumatoid arthritis | Suppressed arthritis development in humanized mice, opposite to the pro-inflammatory P. copri.[3] |
| Psoriasis and atopic dermatitis (EDP1815) | As the single-strain therapeutic EDP1815, it showed anti-inflammatory effects and signs of clinical efficacy in Phase 1b trials, with placebo-like safety and no immunosuppression.[2] |
P. histicola is a beneficial commensal and an investigational therapeutic, not an infection to clear; the entries below are classified by our validation method and are not medical advice.
| Intervention | Class | Status |
|---|---|---|
| EDP1815 (single-strain oral microbial medicine) | Live biotherapeutic | Validation In Progress |
| P. histicola as a next-generation probiotic | Probiotic | Validation In Progress |
| Anti-inflammatory, fiber-rich dietary pattern | Diet | Validation In Progress |
| Intervention | Mechanism |
| EDP1815 | A gut-restricted, non-colonizing single strain that signals from the gut to reduce Th1, Th2, and Th17 inflammation body-wide, without systemic exposure or microbiota change.[2] |
| Probiotic use | Delivering P. histicola aims to expand regulatory T cells and dampen autoimmune inflammation, as shown in disease models.[1] |
| Anti-inflammatory diet | Supporting anti-inflammatory commensals broadly favors the tolerant gut state in which P. histicola is associated with health.[4] |
Where Prevotella histicola (NCBI:txid470565) 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 29 conditions and 32 studies, the signal is genuinely mixed: enriched in 11, depleted in 16, and direction-conflicting in 2 (directional agreement 0.58). Because P. histicola is an anti-inflammatory, health-associated commensal, depletion in an inflammatory or autoimmune group is the more mechanistically interpretable direction, so the aggregate evidence tier is Low.
How to read these. P. histicola behaves as a marker of an anti-inflammatory, tolerant gut, so a drop in an autoimmune or inflammatory cohort is the expected, interpretable signal. Because the Prevotella genus mixes pro- and anti-inflammatory species, species-level resolution matters, and direction can vary by cohort, which is why the aggregate tier stays Low.
Internal summaries of the 32 studies we reviewed in which P. histicola was a differential taxon across this corpus.
Repeated semiannual azithromycin mass drug administration (MDA) to children has been shown to reduce all-cause childhood mortality. However, antibiotic resistance is a major public health concern as the program is being implemented in sub-Saharan Africa. In the double-blind, cluster-randomized, placebo-controlled trial (AVENIR) in Niger, we evaluated the impact of azithromycin MDA targeting different age groups on mortality and on the gut and nasopharyngeal microbiome and resistome of children in participating communities. A total of 3,000 communities were randomized in a 1:1:1 allocation to 3 arms: 2 years of semiannual MDA of (1: child-azithromycin) azithromycin to 1-59-month olds, (2: infant-azithromycin) azithromycin to 1-11-month olds and placebo to 12-59-month olds or (3: placebo) placebo to 1-59-month olds. Mortality (co-primary endpoint) and safety data have previously been published. Here we report on resistance (the co-primary endpoint). One hundred fifty communities (50 per arm) were selected for this analysis. A total of 4,382 rectal and 4,402 nasopharyngeal samples were included. The co-primary outcomes included changes in gut and nasopharynx macrolide AMR. The trial met its primary AMR endpoint for the gut but not for the nasopharynx. The gut macrolide AMR burden in fold change between arms was highest in child-azithromycin compared with placebo (1.16, 95% confidence interval (CI): 1.06-1.28; P < 0.01), followed by child-azithromycin compared with infant-azithromycin (1.13, 95% CI: 1.02-1.23; P = 0.01), and infant-azithromycin compared with placebo (1.04×, 95% CI: 0.94-1.15×; P = 0.66). There were no statistically significant differences in macrolide AMR selection fold change in the nasopharynx between arms: 2.14 (95% CI: 0.93-4.99) for child-azithromycin versus placebo, 2.08 (95% CI: 0.93-4.69) for infant-azithromycin versus placebo, and 1.03 (95% CI: 0.46-2.30) for child-azithromycin versus infant-azithromycin. Close monitoring of AMR should be an essential component of MDA for childhood mortality. ClinicalTrials.gov registration: NCT04224987.
Species in the family Canidae occupy different spatial ecological niches, and some (e.g., wolf) can be kept in zoos. The gut microbiome may differ among various wild and captive canids. Therefore, we compared the gut microbiomes of wild canids (wolf, red fox, and corsac fox) in the Hulun Lake area, captive wolves, and domestic dogs in different regions using metagenomic data. A random forest analysis revealed significant enrichment for bacterial species producing short-chain fatty acids and the thermogenesis pathway (ko04714) in the gut microbiome of wild wolf, potentially providing sufficient energy for adaptation to a wide range of spatial ecological niches. The significantly enriched bacterial species and functional pathways in the gut microbiome of corsac foxes were related to physiological stability and adaptation to arid environments. Alpha diversity of carbohydrate-active enzymes in the gut microbiome was higher in the red fox than in the corsac fox and wild wolf, which may be related to the abundance of plant seeds (containing carbohydrates) in their diets (red foxes inhabit seed-rich willow bosk habitats). However, the influence of host genetic factors cannot be excluded, and further experimental studies are needed to verify the study results. In addition, captive environments drove similarity in carbohydrate-active enzymes (CAZymes) and virulence factors (VFs) in the gut microbiomes of captive wolf and domestic dog, and increased the diversity of CAZymes and VFs in the gut microbiome of captive wolf. Increased VFs diversity may increase the pathogenic potential of the gut microbiome in captive wolves. Therefore, it is necessary to continue monitoring the health status of captive wolves and develop appropriate management strategies.
Researchers compared the salivary microbiome and metabolome of 30 children with severe early childhood caries (S-ECC) against 30 caries-free children. The goal was to characterize ecological and metabolic shifts underlying S-ECC and identify candidate biomarkers.
Saliva samples underwent high-throughput 16S rRNA gene sequencing paired with untargeted metabolomics. Investigators identified differential taxa and metabolites, ran KEGG pathway enrichment, and performed integrated correlation analysis linking key bacteria to specific metabolites.
S-ECC saliva was enriched in Rothia, Lautropia, Lactobacillus, Achromobacter, Streptococcus mutans, Prevotella histicola, and Lachnoanaerobaculum saburreum, while Bergeyella and Acinetobacter were more abundant in caries-free children. Of 4,325 detected metabolites, 1,226 differed significantly, with amino acid metabolism metabolites (phenylalanine, tyrosine, arginine, proline, D-amino acids, aminobenzoate) upregulated in S-ECC. S. mutans, P. histicola, and L. saburreum correlated positively with metabolites including succinic acid, 2-piperidone, D-3-phenyllactic acid, and L-valine.
The paired microbiome-metabolome signature, especially amino acid metabolism alterations, points to potential biomarkers for early detection and targeted intervention in S-ECC. The authors note the cross-sectional, single-time-point design limits conclusions about disease progression, calling for longitudinal follow-up.
This study examined the microbial composition and temporal dynamics of the human microbiome at four body sites: stool, oral, skin, and nasal. The researchers tracked how these microbial communities changed over time and how they related to host multi-omics data, immune markers, and clinical features. The goal was to understand how the microbiome behaves dynamically during both health and disease.
The study followed 86 participants over a period of 6 years, sampling microbiomes from four body sites in each person. The abstract does not specify additional demographic details such as age range or sex distribution. Some participants in the cohort were insulin-resistant, allowing comparison between metabolically healthy and metabolically disrupted individuals.
Microbiome stability and individuality were found to be body-site specific and strongly shaped by the host, with the stool and oral microbiomes proving more stable than the skin and nasal microbiomes, likely due to differing levels of interaction with the host and external environment. The researchers identified both individual-specific and commonly shared bacterial taxa, and individualized taxa showed greater stability over time. Notably, microbiome dynamics were correlated across different body sites, pointing to systemic patterns driven by host-microbial-environment interactions. Insulin-resistant individuals showed altered microbial stability and disrupted associations among microbiome composition, molecular markers, and clinical features.
The findings suggest that microbiome stability is not uniform across the body and that host factors play a central role in shaping which microbial communities remain stable versus dynamic over time. The correlation of microbiome dynamics across separate body sites implies a systemic, whole-body relationship between host and microbiota rather than site-isolated behavior. The disrupted microbiome-host associations seen in insulin resistance suggest that metabolic disease may involve a breakdown in normal host-microbial coupling, offering a potential angle for understanding or monitoring metabolic disease through longitudinal microbiome tracking.
Researchers compared the oral microbiome of Alzheimer's disease (AD) patients (n = 64) to cognitively healthy seniors (n = 71) in Central Asia. They used 16S ribosomal RNA sequencing to characterize bacterial taxonomic composition in each group.
This was a case-control study. Oral samples were sequenced and analyzed for taxonomic composition, diversity, and functional metabolic pathways, then compared between the AD and healthy groups. A separate region-based analysis compared oral microbiome differences within the AD cohort.
The AD group had higher overall microbial diversity, with an increase in Firmicutes and a decrease in Bacteroidetes compared to healthy seniors. LEfSe analysis identified distinct genus-level differences between groups, and periodontitis-associated bacteria were decreased in the AD group. Metabolic pathway distributions also differed notably between the two groups, though bacterial richness and functional differences were absent in the region-based comparison.
The findings support a link between periodontal disease, oral microbiome alterations, and Alzheimer's disease. The authors note that a complete picture of oral microbiome composition in AD still requires further investigation.
Translational microbiome research using next-generation DNA sequencing is challenging due to the semi-qualitative nature of relative abundance data. A novel method for quantitative analysis was applied in this 12-week clinical trial to understand the mechanical vs. chemotherapeutic actions of brushing, flossing, and mouthrinsing against the supragingival dental plaque microbiome. Enumeration of viable bacteria using vPCR was also applied on supragingival plaque for validation and on subgingival plaque to evaluate interventional effects below the gingival margin.
Subjects with gingivitis were enrolled in a single center, examiner-blind, virtually supervised, parallel group controlled clinical trial. Subjects with gingivitis were randomized into brushing only (B); brushing and flossing (BF); brushing and rinsing with Listerine® Cool Mint® Antiseptic (BA); brushing and rinsing with Listerine® Cool Mint® Zero (BZ); or brushing, flossing, and rinsing with Listerine® Cool Mint® Zero (BFZ). All subjects brushed twice daily for 1 min with a sodium monofluorophosphate toothpaste and a soft-bristled toothbrush. Subjects who flossed used unflavored waxed dental floss once daily. Subjects assigned to mouthrinses rinsed twice daily. Plaque specimens were collected at the baseline visit and after 4 and 12 weeks of intervention. Bacterial cell number quantification was achieved by adding reference amounts of DNA controls to plaque samples prior to DNA extraction, followed by shallow shotgun metagenome sequencing.
286 subjects completed the trial. The metagenomic data for supragingival plaque showed significant reductions in Shannon-Weaver diversity, species richness, and total and categorical bacterial abundances (commensal, gingivitis, and malodor) after 4 and 12 weeks for the BA, BZ, and BFZ groups compared to the B group, while no significant differences were observed between the B and BF groups. Supragingival plaque vPCR further validated these results, and subgingival plaque vPCR demonstrated significant efficacy for the BFZ intervention only.
This publication reports on a successful application of a quantitative method of microbiome analysis in a clinical trial demonstrating the sustained and superior efficacy of essential oil mouthrinses at controlling dental plaque compared to mechanical methods. The quantitative microbiological data in this trial also reinforce the safety and mechanism of action of EO mouthrinses against plaque microbial ecology and highlights the importance of elevating EO mouthrinsing as an integral part of an oral hygiene regimen.
This study investigated the relationship between periodontitis and the oral-gut axis in first-trimester pregnant women using integrative microbiome and metabolome profiling. Researchers combined 16S rRNA sequencing of subgingival plaque, saliva, and stool with untargeted metabolomics of serum and other sample types, alongside clinical traits. The goal was to characterize how oral dysbiosis linked to periodontitis translates into distal gut microbial and metabolic changes during early pregnancy.
The cohort consisted of 54 Chinese pregnant women sampled at the first trimester. Of these, 31 women had maternal periodontitis (the Perio group) and 23 women served as Non-Perio controls. Subgingival plaque, saliva, serum, and stool samples were collected from each participant for multi-omics analysis.
The study identified a novel bacterial distinguisher, Coprococcus, in the feces of women with periodontitis, and this genus was associated with subgingival periodontopathogens. Notably, Coprococcus behaved differently from other fecal genera within the Lachnospiraceae family. The ratio of fecal Coprococcus to Lachnoclostridium was able to discriminate between the Perio and Non-Perio groups, indicating a measurable gut-level signature tied to oral disease status.
The findings support the existence of a functional oral-gut axis through which periodontitis in early pregnancy is reflected in distinct gut microbial and metabolic alterations. Identifying the fecal Coprococcus to Lachnoclostridium ratio as a discriminating feature suggests potential translational value as a biomarker linking oral and gut health in pregnant women. This integrative multi-omics approach may help clarify how periodontitis contributes to adverse pregnancy outcomes via systemic, gut-mediated pathways.
This study aimed to compare the gut and oral microbiota composition of professional male football players and amateurs. Environmental and behavioral factors are well known to modulate intestinal microbiota composition. Active lifestyle behaviors are involved in the improvement of metabolic and inflammatory parameters. Exercise promotes adaptational changes in human metabolic capacities affecting microbial homeostasis. Twenty professional football players and twelve amateurs were invited to the study groups. Fecal and oral microbiota were analyzed using next-generation sequencing of the 16S rRNA gene. Diversity in the oral microbiota composition was similar in amateurs and professionals, while the increase in training intensity reduced the number of bacterial species. In contrast, the analysis of the intestinal microbiota showed the greatest differentiation between professional football players and amateurs, especially during intensive training. Firmicutes were characterized by the largest population in all the studied groups. Intensive physical activity increases the abundance of butyrate and succinate-producing bacteria affecting host metabolic homeostasis, suggesting a very beneficial role for the host immune system's microbiome homeostasis and providing a proper function of the host immune system.
This study examined whether the composition of the oral microbiome is linked to autism spectrum disorder (ASD) and neurodevelopmental outcomes. Researchers used large-scale metagenomic sequencing of saliva samples to test whether microbial community differences could distinguish ASD subjects from neurotypical individuals. They also examined whether microbiome composition correlated with cognitive impairment (measured by IQ) and whether microbial strain sharing between children and parents differed by diagnosis and IQ status. A functional enrichment analysis was performed to identify metabolic pathways that might underlie these differences.
The study drew on more than 7000 whole-genome sequenced salivary samples from 2025 US families that included children diagnosed with ASD. Each family contributed samples from both an ASD-diagnosed child and a neurotypical sibling (NT), allowing within-family comparisons. This is a large, family-based cross-sectional cohort rather than a small clinical sample.
Oral microbiome composition discriminated ASD children from their neurotypical siblings with an AUC of 0.66, based on 108 differentiating species (q < 0.005). The relative abundance of these species was highly correlated with Full-Scale IQ, and ASD children with IQ below 70 showed significantly lower microbiome strain sharing with their parents than neurotypical children (p < 10-6). Functional enrichment analysis pointed to enzymes involved in serotonin, GABA, and dopamine degradation pathways as contributors to the distinct microbial community differences between ASD and NT samples. Restrictive eating patterns and oral hygiene proxies had only minor effects on these microbiome differences.
The findings support oral microbiome composition, including neurotransmitter-degradation pathway activity, as a candidate biological marker associated with ASD and its severity as measured by IQ. The reduced strain sharing with parents in lower-IQ ASD children suggests altered microbial transmission or colonization dynamics may track with symptom severity. However, the authors note that causal relationships could not be established, and residual lifestyle differences between groups may still explain part of the association, so these results should be viewed as correlational markers rather than proof of a mechanistic link.
This study investigated the role of gut microbiota and their metabolites, particularly short-chain fatty acids (SCFAs), in the pathogenesis of functional constipation (FC). The researchers used shotgun metagenomic sequencing of gut microbiota alongside serum SCFA analysis to examine relationships between microbial composition, butyric acid levels, and defecation frequency. They then tested the direct effects of butyrate on intestinal neurons using an in vitro mouse model to explore a possible mechanistic link between microbial butyrate metabolism and enteric nervous system damage.
The primary cohort consisted of 460 Chinese women with differing defecation frequencies, who underwent shotgun metagenomic sequencing and serum SCFA measurement. Findings were verified in an independent cohort of 6 patients with functional constipation and 6 controls. In addition, mouse intestinal neurons were used in vitro to test the cellular effects of butyrate exposure at concentrations of 0.1, 0.5, 1, and 2.5 mM.
The abundance of Fusobacterium varium, a butyric acid-producing bacterium, was positively correlated with defecation frequency, while serum butyric acid concentration was negatively correlated with defecation frequency. These findings were confirmed in the independent validation cohort. In vitro, intestinal neurons treated with 0.5 mM butyrate proliferated better than neurons exposed to other tested concentrations, with significant differences observed in cell cycle and oxidative phosphorylation signaling pathways.
The findings suggest that abnormal butyrate metabolism, including altered production by gut bacteria such as Fusobacterium varium and shifts in serum butyrate levels, may damage the enteric nervous system and contribute to functional constipation. This points to butyrate-modulating microbes and serum butyrate concentration as potential biomarkers or targets for understanding and managing FC. It also highlights that butyrate's effect on enteric neurons is concentration-dependent, meaning both insufficient and excessive levels may be relevant to disease mechanisms.
This study investigated the duodenal mucosa-associated microbiota and its surrounding microenvironment in relation to hyperglycemia, an area far less studied than stool microbiota in metabolic disease. The researchers compared paired stool and duodenal microbial samples between hyperglycemic and normoglycemic individuals. They also assessed the duodenal microenvironment directly by measuring tissue oxygen saturation, serum inflammatory markers, and zonulin as a marker of gut permeability. The goal was to determine whether duodenal, rather than stool, microbial changes track more closely with glycemic status.
The study population consisted of 33 subjects with hyperglycemia, defined as HbA1c of 5.7% or higher and fasting plasma glucose above 100 mg/dl, compared against 21 normoglycemic subjects. Both groups contributed paired stool and duodenal samples, allowing direct comparison of microbiota across two body sites within the same individuals. No further demographic details are given in the abstract.
Hyperglycemic subjects had a significantly higher duodenal bacterial count than normoglycemic subjects, along with increased pathobionts and reduced beneficial flora. This bacterial overload correlated with elevated serum zonulin and higher TNF-alpha, suggesting a link to increased gut permeability and inflammation. The hyperglycemic group also showed reduced duodenal oxygen saturation, higher total leukocyte count, and lower IL-10, indicating a systemic proinflammatory state. Notably, unlike stool flora, duodenal bacterial profile variability was specifically associated with glycemic status.
These findings suggest the duodenal microbiome and its local microenvironment, rather than stool alone, may play a distinct role in the pathogenesis of hyperglycemia and prediabetes. The association between bacterial overload, reduced oxygen saturation, and systemic inflammatory markers points to a possible mechanistic pathway linking small intestinal dysbiosis to metabolic dysfunction. This work highlights the duodenum as an underexplored but potentially important site for understanding and possibly intervening in early glycemic disturbances.
Treating oral squamous cell carcinoma (OSCC) introduces new ecological environments in the oral cavity. This is expected to cause changes in the oral microbiome. The purpose of this study was to gain new information on the salivary microbiome of OSCC patients in order to improve the aftercare of OSCC patients. The aims of this study were to investigate possible changes in the salivary microbiome profiles of OSCC patients before and after cancer treatment and to compare these changes with the profiles of healthy controls.
Paraffin-stimulated whole saliva samples were collected, and the salivary flow rate was measured from 99 OSCC patients prior to surgical resection of the tumor and other adjuvant therapy. After treatment, 28 OSCC patients were re-examined with a mean follow-up time of 48 months. In addition, 101 healthy controls were examined and sampled. After DNA extraction and purification, the V4 hypervariable region of the 16S rRNA gene was amplified and sequenced using Illumina MiSeq. The merged read pairs were denoised using UNOISE3, mapped to zero-radius operational taxonomic units (zOTUs), and the representative zOTU sequences were assigned a taxonomy using HOMD. Descriptive statistics were used to study the differences in the microbial profiles of OSCC patients before and after treatment and in comparison to healthy controls.
At baseline, the OSCC patients showed a higher relative abundance of zOTUs classified as Streptococcus anginosus, Abiotrophia defectiva, and Fusobacterium nucleatum. The microbial profiles differed significantly between OSCC patients and healthy controls (F = 5.9, p < 0.001). Alpha diversity of the salivary microbiome of OSCC patients was decreased at the follow-up, and the microbial profiles differed significantly from the pre-treatment (p < 0.001) and from that of healthy controls (p < 0.001).
OSCC patients' salivary microbiome profile had a higher abundance of potentially pathogenic bacteria compared to healthy controls. Treatment of the OSCC caused a significant decrease in alpha diversity and increase in variability of the salivary microbiome, which was still evident after several years of follow-up. OSCC patients may benefit from preventive measures, such as the use of pre- or probiotics, salivary substitutes, or dietary counseling. Video Abstract.
This study examined whether the COVID-19 mRNA vaccine BNT162b2 changes the composition of human breast milk microbiota during a two-dose vaccination regimen. It also examined how any such changes relate to the levels of SARS-CoV-2 spike-specific antibodies present in breast milk. The researchers tracked antibody levels and microbiota composition across several time points relative to vaccination, motivated by concerns that maternal mRNA vaccination could affect the breast milk microbiome that helps shape the early-life infant microbiome.
The study enrolled 49 lactating mothers from Hong Kong who received two doses of the BNT162b2 mRNA vaccine between June 2021 and August 2021. Each participant self-collected breast milk samples at four time points: before vaccination, one week after the first dose, one week after the second dose, and one month after the second dose. The abstract does not report additional demographic details about the cohort.
Levels of SARS-CoV-2 spike-specific IgA and IgG in breast milk peaked one week after the second vaccine dose, then rapidly waned, with IgA returning to baseline by one month post-second dose. The richness and overall composition of breast milk microbiota changed dynamically across the vaccination timeline. However, the abundance of beneficial microbes such as Bifidobacterium species did not significantly change following vaccination. The abstract does not mention Bacteroides fragilis, polysaccharide A, or the B. fragilis toxin, so these are not part of this study's findings.
The findings suggest that maternal BNT162b2 vaccination generates a transient but measurable antibody response in breast milk that could offer newborns temporary passive immunity to SARS-CoV-2. The preservation of beneficial Bifidobacterium abundance despite shifts in overall microbiota composition suggests the vaccine does not compromise a key beneficial component of the breast milk microbiome. These results may help reassure lactating mothers and clinicians about the microbiome safety of mRNA vaccination during lactation, while the observed waning of antibodies points to a limited window of passive protection for infants.
Researchers characterized the gut microbiome of Angolan children with sickle cell anaemia (SCA), comparing it to healthy siblings as controls. This was the first microbiota analysis conducted in an Angolan paediatric population with sickle cell disease.
The team collected 72 stool samples from children aged 3 to 14 years, 36 with SCA and 36 healthy siblings. Bacterial 16S rRNA gene sequencing was performed and taxonomic differences were tested with Welch's test.
Children with SCA had significantly more Actinobacteria (5.47% versus 3.25% in siblings, p = 0.013) and more Coriobacteriaceae, a family within that phylum (p = 0.042). At the genus level, Clostridium cluster XI bacteria was more prevalent in SCA children, while siblings showed higher Blautia, Aestuariispira, Campylobacter, Helicobacter, Polaribacter and Anaerorhabdus.
The gut microbiome is thought to drive inflammation and aged-neutrophil production that fuel vaso-occlusive crises in sickle cell disease. Documenting these microbial differences supports future exploration of probiotics, prebiotics or faecal microbiota transfer as adjunct therapies, though the authors stress more research is needed.
Down syndrome (DS), a most frequently occurring genetic disorder, is associated with oral morphological abnormalities and higher incidence rates of oral diseases. Recent studies have analyzed the oral microbiome to elucidate their relationships with oral diseases and general health; however, reports on the oral microbiome in individuals with DS are scarce. This study aimed to characterize the oral microbiome in children with DS.
A total of 54 children aged 1-13 years were enrolled in this case-control study. Of these children, 27 had DS (Case: DS group) and 27 were age-matched healthy children (Control: ND group). Saliva in the oral cavity was collected with a swab, cultured, and tested for cariogenic and periodontopathic bacteria by quantitative polymerase chain reaction (qPCR) detection, and the salivary microbiome was analyzed using next-generation sequencing. The student's t-test, Fisher's exact test, Mann-Whitney U test, and permutational multivariate analysis of variance were used for statistical analysis.
Results of culture and qPCR detection tests for cariogenic and periodontopathic bacteria showed no significant differences in the detected bacteria between the DS and ND groups, with the exception of a significantly higher detection rate of Candida albicans in children with DS with mixed dentition. A comparison of the salivary microbiomes by 16S sequencing showed no significant difference in α diversity; however, it showed a significant difference in β diversity. Children with DS had a higher relative abundance of Corynebacterium and Cardiobacterium, and lower relative abundance of TM7.
This study provided basic data on the salivary microbiome of children with DS and showed the microbiological markers peculiar to children with DS. However, further research to identify the relationship with oral diseases is warranted.
Researchers compared throat-swab oral microbiomes in three groups of men who have sex with men: 15 with acute HIV infection, 15 with chronic HIV infection, and 15 HIV-uninfected controls.
Throat swabs were collected at recruitment (week 0) and again 12 weeks after starting antiretroviral therapy (week 12). Genomic DNA was extracted and analyzed by 16S rRNA gene sequencing.
Microbiome diversity was significantly lower in both acute and chronic HIV infection than in controls, at week 0 and still at week 12. Unidentified Prevotellaceae increased in both infected groups, along with Prevotella in acute infection and Streptococcus in chronic infection, while controls had more Lactobacillus, Rothia, Lautropia, and Bacteroides. After ART, Bradyrhizobium increased in both infected groups, whereas controls showed enrichment of Lactobacillus, Rothia, Clostridia, Actinobacteria, and Ruminococcaceae. Lower CD4+ T-cell counts (under 200 cells per mm3) were linked to lower Haemophilus, Actinomyces, unidentified Ruminococcaceae, and Rothia.
The findings suggest HIV infection and antiretroviral therapy both reshape the oral microbiome, which could inform strategies to improve oral health in people living with HIV.
Bacterial-viral interactions in saliva have been associated with morbidity and mortality for respiratory viruses such as influenza and SARS-CoV. However, such transkingdom relationships during SARS-CoV-2 infection are currently unknown. Here, we aimed to elucidate the relationship between saliva microbiota and SARS-CoV-2 in a cohort of newly hospitalized COVID-19 patients and controls. We used 16S rRNA sequencing to compare microbiome diversity and taxonomic composition between COVID-19 patients (n = 53) and controls (n = 59) and based on saliva SARS-CoV-2 viral load as measured using reverse transcription PCR (RT-PCR). The saliva microbiome did not differ markedly between COVID-19 patients and controls. However, we identified significant differential abundance of numerous taxa based on saliva SARS-CoV-2 viral load, including multiple species within Streptococcus and Prevotella. IMPORTANCE Alterations to the saliva microbiome based on SARS-CoV-2 viral load indicate potential biologically relevant bacterial-viral relationships which may affect clinical outcomes in COVID-19 disease.
The association of taste genetics and the oral microbiome in autoimmune diseases such as rheumatoid arthritis (RA) has not been reported. We explored a novel oral mucosal innate immune pathway involving the bitter taste G protein-coupled receptor T2R38. This case-control study aimed to evaluate whether T2R38 polymorphisms associate with the buccal microbial composition in RA. Genomic DNA was obtained from buccal swabs of 35 RA patients and 64 non-RA controls. TAS2R38 genotypes were determined by Sanger sequencing. The buccal microbiome was assessed by Illumina MiSeq sequencing of the V4-16S rRNA gene. Bacterial community differences were analyzed with alpha and beta diversity measures. Linear discriminant analysis effect size identified taxa discriminating between RA versus non-RA and across TAS2R38 genotypes. TAS2R38 genotype frequency was similar between RA and non-RA controls (PAV/PAV; PAV/AVI; AVI/AVI: RA 42.9%; 45.7%; 11.4% versus controls 32.8%; 48.4%; 18.8%, chi-square (2, N = 99) = 2.1, p = 0.35). The relative abundance of Porphyromonas, among others, differed between RA and non-RA controls. The relative abundance of several bacterial species also differed across TAS2R38 genotypes. These findings suggest an association between T2R38 polymorphisms and RA buccal microbial composition. However, further research is needed to understand the impact of T2R38 in oral health and RA development.
The purpose of the present study was to characterize the composition of the salivary microbiota and quantify salivary levels of inflammation-related proteins (neutrophil gelatinase-associated lipocalin [NGAL] and transferrin) in patients with psoriasis and compare data to those obtained in patients with periodontitis and orally healthy controls, respectively.
Stimulated saliva samples from patients with psoriasis (n = 27), patients with periodontitis (n = 58), and orally healthy controls (n = 52) were characterized by means of next-generation sequencing of the 16S rRNA gene. Salivary levels of NGAL and transferrin were quantified using immunoassays.
Linear discriminant effect size analysis showed that 52 (22 psoriasis-associated and 30 periodontitis-associated) and 21 (8 psoriasis-associated and 13 orally healthy control-associated) bacterial taxa differentiated the salivary microbiota in patients with psoriasis from that of patients with periodontitis and orally healthy controls, respectively. Significantly lower mean salivary levels of NGAL (psoriasis: 996 [std. error 320], periodontitis: 2,072 [295], orally healthy controls: 2,551 [345] ng/ml, p < .0001) and transferrin (psoriasis: 4.37 [0.92], periodontitis: 7.25 [0.88], orally healthy controls: 10.02 [0.94] ng/ml, p < .0001) were identified in patients with psoriasis.
Psoriasis associates with characteristics of the salivary microbiota and salivary levels of inflammation-related proteins, which are different from characteristics in patients with periodontitis and orally healthy controls, respectively.
This study examined the gut microbiota structure of children with Autism Spectrum Disorder (ASD) across different ages and its relationship to fecal metabolites. Researchers used 16S rRNA sequencing to characterize the gut microbial population, then applied metagenomics and liquid chromatography-mass spectrometry to investigate a subset with chronic constipation. The goal was to clarify how gut microbial composition and its metabolic activity relate to ASD and to the gastrointestinal symptoms that commonly accompany it.
The primary cohort consisted of 143 children aged 2 to 13 years old, evaluated using 16S rRNA sequencing and grouped into ASD and typically developing (TD) categories. A subset of 30 children with ASD and co-occurring chronic constipation (C-ASD), along with their age-matched TD counterparts, was selected for more detailed metagenomic and metabolomic analysis. No further demographic or geographic details were provided in the abstract.
The ASD group showed no significant increase in gut microbial diversity with age, unlike the TD group, whose diversity increased as children got older, indicating a divergent developmental trajectory of the gut microbiota in ASD. Among children with constipation, the C-ASD group had decreased microbial diversity and depletion of Sutterella, Prevotella, and Bacteroides compared to matched TD children. These compositional changes were accompanied by dysregulated metabolism activities, and metabolomic analysis using liquid chromatography-mass spectrometry supported the metagenomic findings, though the abstract text was truncated before further detail.
The findings suggest that gut microbiota development in ASD does not follow the same age-related maturation seen in typically developing children, pointing to a distinct trajectory that may reflect or contribute to disease biology. The depletion of specific genera and disrupted metabolic activity in constipated ASD children implicate the gut microbiome in the pathogenesis of gastrointestinal symptoms that frequently co-occur with ASD. These results support the gut microbiota and its metabolic output as a potential area for further mechanistic study and biomarker development in ASD subgroups with GI involvement.
Background: Oral mucositis (OM) is a common side effect of conditioning therapy implemented before hematopoietic stem cell transplantation (HSCT). The role of oral microbiome in OM is not fully elucidated. Objective: To determine oral microbiome profile changes post-conditioning in HSCT patients who developed moderate OM, or mild to no OM. Design: Patient groups were: Muc0-1 with OM-score = 0-1 (43 paired samples) and Muc2 with WHO OM-score = 2 (36 paired samples). Bacterial DNA was isolated from oral samples (saliva, swabs of buccal mucosa, tongue, and supragingival plaque) at pre-conditioning (T 0 ), post-conditioning mucositis onset (T Muc ), and one-year post-conditioning (T Year ). 16S-rRNA gene next-generation sequencing was used to determine the relative abundance (RA) of >700 oral species. Alpha-diversity, beta-diversity and linear discriminant analyses (LDA) were performed Muc2 versus Muc0-1. Results: Muc2 oral microbiome alpha- and beta-diversity differed between T 0 and T Muc . Muc2 alpha-diversity and Muc0-1 beta-diversity did not differ between T 0 and T Year . T 0 to T Muc LDA scores were significant in Muc2 for Gammaproteobacteria. For Muc2 patients, the average RA decreased for Haemophilus parainfluenza, a species known as mucosal surfaces protector, but increased for Escherichia-Shigella genera. Conclusions: Post-conditioning OM might contribute to long-term oral microbiome changes affecting Gammaproteobacteria, in HSCT patients.
This study characterized the gut microbiota of patients with advanced primary hepatocellular carcinoma (HCC) who received immune checkpoint inhibitors (ICIs). Researchers amplified and sequenced the 16S rDNA V4 region on the MiSeq platform to profile bacterial composition. The goal was to determine whether specific gut bacterial taxa relate to how patients respond to ICI treatment.
The study drew on an initial cohort of 65 patients with metastatic melanoma who were treated with ICIs at Fujian provincial geriatric hospital between August 2016 and June 2018. This cohort was used in the context of a larger Chinese population-based study of HCC patients with hepatitis B virus infection who received ICIs. Patients were later stratified into high versus low groups based on the median relative abundance of specific bacterial taxa in their gut microbiome.
Gut microbiota diversity was found to be notably increased in HCC patients who received ICIs, a pattern attributed to negative feedback between microbial metabolic activity and host pathways. The Faecalibacterium genus was highlighted in the response group, while the Bacteroidales order stood out in the non-response group. Patients with high Faecalibacterium abundance had significantly prolonged progression-free survival (PFS) compared to those with low abundance.
These findings suggest that gut microbiota composition, particularly Faecalibacterium abundance, may serve as a biomarker for predicting response and progression-free survival in HCC patients treated with immune checkpoint inhibitors. Because Faecalibacterium prausnitzii is a recognized butyrate-producing, anti-inflammatory commensal, its association with better outcomes points to a possible link between gut-derived anti-inflammatory activity and immunotherapy efficacy. This raises the possibility that modulating gut microbiota could become a strategy to improve ICI outcomes in liver cancer, though further studies are needed to establish causality.
An association between the vaginal microbiota and preterm birth (PTB) has been reported in several research studies. Population shifts from high proportions of lactobacilli to mixed species communities, as seen with bacterial vaginosis, have been linked to a twofold increased risk of PTB. Despite the increasing number of studies using next-generation sequencing technologies, primarily involving 16S rRNA-based approaches, to investigate the vaginal microbiota during pregnancy, no distinct microbial signature has been associated with PTB. Shotgun metagenomic sequencing offers a powerful tool to reveal community structures and their gene functions at a far greater resolution than amplicon sequencing. In this study, we employ shotgun metagenomic sequencing to compare the vaginal microbiota of women at high risk of preterm birth (n = 35) vs. a low-risk control group (n = 14). Although microbial diversity and richness did not differ between groups, there were significant differences in terms of individual species. In particular, Lactobacillus crispatus was associated with samples from a full-term pregnancy, whereas one community state-type was associated with samples from preterm pregnancies. Furthermore, by predicting gene functions, the functional potential of the preterm microbiota was different from that of full-term equivalent. Taken together, we observed a discrete structural and functional difference in the microbial composition of the vagina in women who deliver preterm. Importance: with an estimated 15 million cases annually, spontaneous preterm birth (PTB) is the leading cause of death in infants under the age of five years. The ability to accurately identify pregnancies at risk of spontaneous PTB is therefore of utmost importance. However, no single cause is attributable. Microbial infection is a known risk factor, yet the role of vaginal microbes is poorly understood. Using high-resolution DNA-sequencing techniques, we investigate the microbial communities present in the vaginal tracts of women deemed high risk for PTB. We confirm that Lactobacillus crispatus is strongly linked to full-term pregnancies, whereas other microbial communities associate with PTB. Importantly, we show that the specific functions of the microbes present in PTB samples differs from FTB samples, highlighting the power of our sequencing approach. This information enables us to begin understanding the specific microbial traits that may be influencing PTB, beyond the presence or absence of microbial taxa.
Researchers compared the saliva microbiome of 10 women with polycystic ovary syndrome (PCOS) and 10 healthy controls across a full day. Salivary samples were also compared against each participant's fecal microbiota.
16S rRNA gene amplicon sequencing was run on saliva and stool samples, with saliva collected every 6 hours over 24 hours (Zeitgeber 0, 6, 12, and 18).
At every time point, PCOS saliva samples differed significantly from controls in taxa and metabolic pathways. Healthy women showed a diurnal rhythm in salivary microbiota abundance, but this rhythm was disrupted in PCOS patients. No comparable diurnal or compositional differences were found in the fecal microbiota between groups.
Loss of the normal daily rhythm in oral microbiota may contribute to oral disease and systemic metabolic disturbances in PCOS, suggesting saliva timing could matter for future biomarker work.
Rheumatoid arthritis (RA) is an autoimmune disease characterized by joint inflammation. Individuals with RA have a higher risk of periodontitis and periodontitis has been linked to RA through the production of enzymes by periodontal pathogens that citrullinate proteins. This linkage is supported by findings that periodontitis is associated with increased RA severity and treatment of periodontitis can improve the symptoms of RA. The possible mechanism for this association is through dysbiosis of the oral microbiota triggered by RA-induced systemic inflammation. We examined the RA status of subjects by measuring the number of tender and swollen joints, anti-citrullinated protein antibody and rheumatoid factor. Periodontal disease status and salivary cytokine levels were measured, and dental plaque analyzed by 16S rRNA high throughput sequencing. RA patients had a higher bacterial load, a more diverse microbiota, an increase in bacterial species associated with periodontal disease, more clinical attachment loss, and increased production of inflammatory mediators including IL-17, IL-2, TNF, and IFN-γ. Furthermore, changes in the oral microbiota were linked to worse RA conditions. Our study provides new insights into the bi-directional relationship between periodontitis and RA and suggest that monitoring the periodontal health of RA patients is particularly important.
Acetaldehyde, associated with consumption of alcoholic beverages, is known to be a carcinogen and to be related to the tongue dorsum. The aim of this study was to investigate the relationship between acetaldehyde concentration in mouth air and bacterial characteristics on the tongue dorsum.
Thirty-nine healthy volunteers participated in the study. Acetaldehyde concentrations in mouth air were evaluated by a high-sensitivity semiconductor gas sensor. A 16S rRNA gene sequencing technique was used to compare microbiomes between two groups, focusing on the six samples with the highest acetaldehyde concentrations (HG) and the six samples with lowest acetaldehyde concentrations (LG).
Acetaldehyde concentration increased in correlation with the increase in bacterial count (p=0.048). The number of species observed in the oral microbiome of the HG was higher than that in the oral microbiome of the LG (p=0.011). The relative abundances of Gemella sanguinis, Veillonella parvula and Neisseria flavescens in the oral microbiome of the HG were higher than those in the oral microbiome of the LG (p<0.05).
Acetaldehyde concentration in mouth air was associated with bacterial count, diversity of microbiome, and relative abundance of G. sanguinis, V. parvula, and N. flavescens.
This study examined how the oral microbiome influences the development of oral squamous cell carcinoma (OSCC), the most common head and neck malignancy worldwide. Using 16S rRNA gene sequencing and metatranscriptomic analysis, researchers tracked longitudinal changes in oral microbiome composition and function in a 4-nitroquinoline-1-oxide (4-NQO)-induced mouse model of OSCC. The work compared gnotobiotic mice colonized with different oral microbiome inocula to mice exposed to 4-NQO without any microbiome present.
The subjects were gnotobiotic (germ-free) mice experimentally colonized with one of two oral microbiome inocula, one sourced from healthy mice and the other from mice bearing a 4-NQO-induced tumor. Controls consisted of mice exposed to 4-NQO but lacking any microbiome colonization. This was an animal model study, not a human cohort, designed to isolate the microbiome's contribution to tumorigenesis.
Mice colonized with an oral microbiome and exposed to 4-NQO developed more tumors and larger tumors than 4-NQO-exposed controls with no microbiome, indicating the microbiome actively promoted tumorigenesis rather than merely accompanying it. Tumorigenic samples showed an overall increase in microbial diversity compared to non-tumor, non-4-NQO-exposed samples. Despite variable community dynamics across groups, consistent patterns emerged during disease progression, including opposite abundance trends for Parabacteroides and Corynebacterium in the two groups inoculated with the OSCC-associated microbiome, with Parabacteroides decreasing in the control group.
The findings suggest the oral microbiome is not a passive bystander in OSCC but an active promoter of tumor initiation and growth, supporting a causal rather than merely correlative role for oral dysbiosis in this cancer. The divergent Parabacteroides and Corynebacterium dynamics point to specific taxa that could serve as markers of tumorigenic risk or as targets for future mechanistic study. Because the model used gnotobiotic mice with defined inocula, it offers a controlled system for further dissecting which microbial functions drive carcinogenesis in the oral cavity.
This study examined whether the oral and gut microbiome influences how melanoma patients respond to anti-PD-1 checkpoint blockade immunotherapy. Researchers compared microbiome diversity, composition, and metagenomic function between patients who responded to treatment and those who did not. They also tested whether transferring the gut microbiome from responding patients could alter antitumor immunity in mice.
The study included 112 melanoma patients undergoing anti-PD-1 immunotherapy, whose oral and gut microbiomes were profiled. A subset of 43 patients had fecal microbiome samples analyzed in detail, comprising 30 responders and 13 nonresponders. Germ-free mice were also used as recipients in fecal transplant experiments from responding patients.
Responding patients had significantly higher gut microbiome alpha diversity and a significantly greater relative abundance of bacteria from the Ruminococcaceae family compared to nonresponders. Metagenomic analysis showed functional differences in the gut bacteria of responders, including enrichment of anabolic pathways. Immune profiling indicated enhanced systemic and antitumor immunity in responding patients with a favorable gut microbiome, and this enhanced immunity was also observed in germ-free mice that received fecal transplants from responders.
These findings suggest the gut microbiome plays a causal role in shaping how melanoma patients respond to immune checkpoint inhibitor therapy, extending prior mouse-model evidence into human cancer patients. The identification of specific compositional and functional microbiome features, such as Ruminococcaceae abundance and enriched anabolic pathways, associated with response points toward potential microbiome-based biomarkers or interventions. This has direct implications for improving outcomes in melanoma patients treated with immune checkpoint inhibitors.
This study investigated whether rheumatoid arthritis (RA) itself alters the subgingival (below-the-gumline) oral microbiome, independent of periodontitis. Prior work linking RA to dysbiotic oral microbiomes had been confounded because those RA patients often also had extensive periodontal disease. Here, researchers isolated the effect of RA by studying only periodontally healthy individuals, comparing those with RA to those without. Subgingival plaque samples underwent 16S rRNA gene sequencing on an Illumina MiSeq platform, and community composition and co-occurrence patterns were analyzed with the QIIME and PhyloToAST bioinformatics pipelines.
The cohort consisted of 41 periodontally healthy individuals: 22 with rheumatoid arthritis and 19 without RA serving as controls. All participants were confirmed periodontally healthy, which removed periodontitis as a confounding variable. The abstract does not provide further demographic details such as age, sex distribution, or geographic origin.
Subgingival microbiomes differed significantly between RA patients and controls, with 41.9% of the community differing in relative abundance and 19% differing in membership (which taxa were present at all). Co-occurrence network analysis showed a striking structural difference: control networks were sparse and made up mostly of congeneric (same-genus) relationships, while RA patient networks formed a highly connected grid anchored by a large intergeneric hub built from known periodontal pathogens. Predictive metagenomic analysis (PICRUSt) suggested that arachidonic acid and ester lipid metabolism pathways may partly explain why this pathogen-anchored network was so tightly clustered in RA patients.
The findings indicate that RA is associated with a distinctly dysbiotic subgingival microbial community structure even in the complete absence of periodontitis, meaning RA itself, not just co-occurring gum disease, may reshape the oral microbiome. The emergence of a periodontal-pathogen-anchored co-occurrence hub in clinically healthy gums suggests these organisms could be functionally primed to promote inflammation before overt disease appears. This supports the oral microbiome, and its lipid-metabolism-linked pathogen networks, as a candidate factor in RA pathogenesis worth further mechanistic and longitudinal investigation.
Researchers assessed the esophageal microbiome of 106 prospectively recruited patients at Prince of Wales Hospital, Sydney, spanning normal esophagus, GERD, glandular mucosa, and Barrett's esophagus. They tested associations between microbiome composition and age, gender, proton pump inhibitor use, host genetics, and disease stage along the esophageal adenocarcinoma cascade.
The team combined 16S rRNA and 18S rRNA amplicon sequencing with shotgun metagenomic sequencing of esophageal brushings. Host single nucleotide polymorphisms were identified from shotgun reads mapped to the human genome and tested for association with microbiome composition using MicrobiomeGWAS, then validated with custom Fluidigm SNP assays.
The esophageal microbiome clustered into three functionally distinct community types, or esotypes, defined by a consistent co-exclusion relationship between Streptococcus and Prevotella. Age significantly shaped microbiome composition, while Gram-negative oral-associated bacteria and microbial lactic acid production pathways (homolactic and heterolactic fermentation) were enriched in GERD and Barrett's esophagus. Bacteriophages were detected in 97.8 percent of subjects, and low-abundance archaea and Candida species were also present. Three host SNPs, in NOTCH2, STEAP2-AS1, and NREP, were validated as associated with microbiome composition.
This is described as the most comprehensive assessment of the esophageal microbiome to date, linking specific bacterial signatures and host genetic markers to early stages of the esophageal adenocarcinoma cascade. The findings identify candidate targets for further investigation in Barrett's esophagus and esophageal adenocarcinoma development.
This study examined the subgingival bacterial biodiversity of untreated chronic periodontitis patients using 16S rRNA gene sequencing. The primary goal was to compare the oral microbiome found in deep, diseased periodontal pockets against shallow, healthy sites. A secondary goal was to assess whether smoking, race, and dental caries influenced this deep-versus-shallow microbial relationship. A universal primer set targeting the V4-V6 region of the 16S rRNA gene was designed to amplify oral microbial sequences.
A total of 88 subjects were recruited from two clinics for this study. From each subject, paired subgingival plaque samples were collected, one from a deep site with probing depth greater than 5 mm and one from a shallow site with probing depth of 3 mm or less. This paired, within-subject design allowed direct comparison of diseased and healthy pocket microbiomes in the same individuals.
Statistical analysis using a two-part model with false discovery rate correction identified 51 of 170 genera and 200 of 746 species that differed significantly in abundance between deep and shallow sites. Beyond bacterial species already known to be associated with periodontal disease, additional species were found to be markedly changed in the diseased, deep sites. Cluster analysis further showed that the degree of microbiome difference between deep and shallow sites was shaped by patient-level factors, including clinic location, race, and smoking status. No sulfate-reducing bacteria, Desulfovibrio, or sulfur-related metabolism were reported in this abstract.
The findings reinforce that chronic periodontitis involves a broad, multi-species shift in subgingival bacterial communities, extending beyond previously recognized periodontal pathogens. Because patient-level factors such as smoking, race, and clinic location influenced the deep-versus-shallow microbiome difference, these variables may need to be accounted for in future periodontal microbiome research and clinical risk assessment. The paired deep-shallow sampling approach offers a model for identifying disease-associated bacterial signatures within the same patient, which could inform future diagnostic or monitoring strategies.
This study looked at how the oral microbiome (the bacteria in the mouth) is affected by human papillomavirus (HPV) infection, especially in people with and without HIV. Researchers analyzed mouth rinse samples from 63 men, comparing their bacterial composition based on whether they had HPV and/or HIV. They found that HPV infection changes the diversity and types of bacteria in the mouth, but these changes were different depending on whether the person also had HIV. In HIV-negative individuals, certain bacteria were more common when HPV was present, while in HIV-positive individuals, different bacterial shifts were observed. The study suggests that HPV infection interacts with the oral microbiome in unique ways, and this interaction may be influenced by HIV status.
2026-07-04
Prevotella histicola majorTaxon page created: biology (morphology, health role, immunomodulatory factors), its ecological role, clinical associations and the EDP1815 program, supportive interventions, the data-derived Conditions table across 29 conditions, and the full research feed.
Shahi SK, Jensen SN, Murra AC, Tang N, Guo H, Gibson-Corley KN, Zhang J, Karandikar NJ, Murray JA, Mangalam AK.
Human commensal Prevotella histicola ameliorates disease as effectively as interferon-beta in the experimental autoimmune encephalomyelitis.Front Immunol. 2020
Itano A, Maslin D, Ramani K, Mehraei G, Carpenter N, Cormack T, Saghari M, Moerland M, Troy E, Caffry W, Wardwell-Scott L, Abel S, McHale D, Bodmer M.
Clinical translation of anti-inflammatory effects of Prevotella histicola in Th1, Th2, and Th17 inflammation.Front Med (Lausanne). 2023
Mangalam AK, Murray J.
Microbial monotherapy with Prevotella histicola for patients with multiple sclerosis.Expert Rev Neurother. 2018
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