Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (537 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The full collection of microbes (bacteria, fungi, virus, etc.) that naturally exist within a particular biological niche such as an organism, soil, a body of water, etc.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Microbiotas; Microbial Community; Community, Microbial; Microbial Communities; Microbial Community Composition; Community Composition, Microbial; Composition, Microbial Community; Microbial Community Compositions.
Where it fits in the MeSH classification
Research landscape
PubMed indexes 128,918 records tagged with the MeSH heading “Microbiota” (counts retrieved 2026-10-31). 94,129 of them (73.0%) were published from 2020 onward, and the busiest period so far is 2020 onward with 94,129 records.
Reviews account for 28,327 records (22.0%) and meta-analyses for 967. Randomized controlled trials number 2,475 (1.9%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 11 |
| 2010-2019 | 36,342 |
| 2020 onward | 94,129 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 28,327 | 22.0% |
| Meta-analyses | 967 | 0.8% |
| Randomized controlled trials | 2,475 | 1.9% |
Method: PubMed query "Microbiota"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in public health and nutrition
Population and nutrition studies mostly observe what people eat, breathe or are exposed to and then look for links with health, which shows association and not proof of cause. Self-reported diet is imprecise, people who eat or live differently also differ in other ways, and effects measured across a population may not apply to one person. Check the study design, how exposure was measured, what else was accounted for and the size of the effect, not only whether it was statistically significant.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Functional Heterogeneity of the Autism Spectrum Disorder-Associated Gut Microbial Ecosystem Revealed by Fecal Lipopolysaccharides and Bacterial Proteomic Profiling | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42809586 · DOI · PMC13623111 |
| Subverting colonization resistance: Salmonella pathogenesis at the interface of microbiota, metabolism and inflammasome | 2026 | Review article Design not recorded in structured metadata | 0 | cc by PMID 42885908 · DOI · PMC13682399 |
| Escherichia coli hns and methylglyoxal link gut microbial metabolism to host neuronal gene regulation in Parkinson's disease | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42878179 · DOI · PMC13679328 |
Functional Heterogeneity of the Autism Spectrum Disorder-Associated Gut Microbial Ecosystem Revealed by Fecal Lipopolysaccharides and Bacterial Proteomic Profiling [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The etiology of pediatric autism spectrum disorder (ASD) has been increasingly linked to alterations in the gut-brain axis, highlighting the intricate bidirectional communication between gut microbiota and central nervous system.
- Closing excerpt
- These findings suggest that gut microbiota in ASD children are associated with a functionally heterogeneous microbial ecosystem characterized by altered immunostimulatory molecular outputs despite the absence of massive taxonomic shifts, with potential relevance for neuroimmune dysregulation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (183 words)
The etiology of pediatric autism spectrum disorder (ASD) has been increasingly linked to alterations in the gut-brain axis, highlighting the intricate bidirectional communication between gut microbiota and central nervous system. The molecular mechanisms of this communication are poorly understood. Here we investigated whether ASD-associated gut microbiota could exhibit altered inflammatory molecular outputs by integrating chemistry-driven profiling of fecal lipopolysaccharides (LPS), functional bacterial proteomics, and neuroimmune cellular assays. Structural analyses revealed that LPS from non-autistic healthy donors (NASD) displayed highly conserved carbohydrate and lipid A signatures dominated by hypo-acylated mono-phosphorylated species typically associated with immunomodulatory Bacteroides-derived LPS. In contrast, LPS from ASD children exhibited increased structural heterogeneity. These molecular alterations were functionally reflected in human HMC3 microglial cells, where ASD-derived fecal LPS induced stronger IL-6 and IL-8 release compared with NASD-derived LPS, indicating enhanced neuroinflammatory potential. Functional proteomic profiling disclosed broadly comparable microbial compositions but marked metabolic divergence. These findings suggest that gut microbiota in ASD children are associated with a functionally heterogeneous microbial ecosystem characterized by altered immunostimulatory molecular outputs despite the absence of massive taxonomic shifts, with potential relevance for neuroimmune dysregulation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42809586 · DOI · PMC13623111
Subverting colonization resistance: Salmonella pathogenesis at the interface of microbiota, metabolism and inflammasome [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The intestinal tract is a key immune organ and microecological system, where colonization resistance (CR) mediated by gut microbiota prevents pathogen invasion.
- Closing excerpt
- We also highlight microbiota-based countermeasures, including probiotics, natural antimicrobials, and phage therapy, as promising strategies to restore gut homeostasis.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (97 words)
The intestinal tract is a key immune organ and microecological system, where colonization resistance (CR) mediated by gut microbiota prevents pathogen invasion. Salmonella disrupts CR via type VI and type III secretion systems (T6SS/T3SS), inducing dysbiosis, inflammasome-driven inflammation, and intestinal barrier damage. This creates a self-reinforcing cycle:dysbiosis alters microbial metabolites, sustains inflammation, and enhances pathogen fitness, favoring chronic infection. This review integrates molecular mechanisms of microbiota disruption, inflammasome activation, and metabolic imbalance to explain how Salmonella overcomes CR. We also highlight microbiota-based countermeasures, including probiotics, natural antimicrobials, and phage therapy, as promising strategies to restore gut homeostasis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42885908 · DOI · PMC13682399
Escherichia coli hns and methylglyoxal link gut microbial metabolism to host neuronal gene regulation in Parkinson's disease [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuron loss in the substantia nigra (SN).
- Closing excerpt
- elegans, with corresponding changes of LSAMP expression in mammalian systems.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (257 words)
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuron loss in the substantia nigra (SN). Although the gut microbiota has been implicated in PD pathogenesis, how defined bacterial genes and their metabolites influence host neuronal gene regulation remains unclear. Here, we identify a gut microbial hns-methylglyoxal (MG) pathway linking Escherichia coli (E. coli) metabolism to host neuronal gene regulation. In the stool metagenomic cohort, hns, a bacterial gene encoding the histone-like nucleoid structuring protein and primarily derived from E. coli, was enriched particularly in body-first PD, a subtype associated with gut-originating pathology. In a separate plasma MG cohort, plasma levels of MG, a reactive metabolite whose bacterial production was hns-dependent in our model system, were higher in body-first than in brain-first PD and were nominally inversely associated with cardiac meta-iodobenzylguanidine (MIBG) uptake within the body-first group. Using Caenorhabditis elegans (C. elegans) PD models, we found that feeding with Δhns E. coli protected dopaminergic neurons, whereas exogenous MG abolished this neuroprotection. Transcriptomic and neuronal RNAi analyses identified rig-5 as a host mediator of hns deletion-induced neuroprotection. Cross-species analyses identified LSAMP as a candidate mammalian ortholog of rig-5. MG suppressed LSAMP expression in human neuronal cells, and LSAMP expression was reduced in the post-mortem SN of patients with PD. Conversely, Lsamp expression was increased in the SN of mice colonized with Δhns E. coli. Together, these findings delineate a microbial gene-metabolite-host gene pathway through which E. coli hns and MG modulate rig-5-dependent dopaminergic vulnerability in C. elegans, with corresponding changes of LSAMP expression in mammalian systems.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42878179 · DOI · PMC13679328
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Association between gut microbiota and preeclampsia-eclampsia: a two-sample Mendelian randomization study [4]
- Research article Oxidative stress gene expression, DNA methylation, and gut microbiota interaction trigger Crohn's disease: a multi-omics Mendelian randomization study [5]
- Research article Host genetic regulation of human gut microbial structural variation [6]
- Research article A gut microbial signature for combination immune checkpoint blockade across cancer types [7]
- Research article Probiotics fortify intestinal barrier function: a systematic review and meta-analysis of randomized trials [8]
- Research article Gut microbiota composition in depressive disorder: a systematic review, meta-analysis, and meta-regression [9]
Full-text reviews on EvidenceLib
Open-access review articles about this topic, reproduced in full with authors, licence and references.
Recent Developments and Applicability of In Vitro Gut Microbiota Models in Biomedical Research and Digestive Diseases—A Systematic Review
Ioana-Miruna Balmus, Gabriel Dascalescu, Viorica Rarinca et al. · Medicina 2026 · CC BY 4.0
The Impact of Plant-Derived Foods and Medicines on the Lung–Gut Axis and Microbiota Cross-Talk
Sarocha Vivatvakin, Duangporn Werawatganon, George Grant · Molecules 2026 · CC BY 4.0
Gut microbiota in poultry: Roles in nutrition, metabolism and production performance
Zhuting Chen, Cheng Xin, Shuang Zhang et al. · Poultry Science 2026 · CC BY 4.0
Skin Microbiota: Mediator of Interactions Between Metabolic Disorders and Cutaneous Health and Disease
Magdalini Kreouzi, Nikolaos Theodorakis, Maria Nikolaou et al. · Microorganisms 2025 · CC BY 4.0
Complementary Feeding and Infant Gut Microbiota: A Narrative Review
Danielle L. Noles, Kinzie L. Matzeller, Daniel N. Frank et al. · Nutrients 2025 · CC BY 4.0
References
- De Chiara S, Di Somma A, Mazziotti V, Coppola S, Oglio F, Tammaro L, et al.. Functional Heterogeneity of the Autism Spectrum Disorder-Associated Gut Microbial Ecosystem Revealed by Fecal Lipopolysaccharides and Bacterial Proteomic Profiling. . 2026. PMID 42809586 · DOI · PMC13623111
- Gao Z, Li Z, Cui J, Zhang Q, Jia Y, Ding K, et al.. Subverting colonization resistance: Salmonella pathogenesis at the interface of microbiota, metabolism and inflammasome. . 2026. PMID 42885908 · DOI · PMC13682399
- Shin MG, Park SJ, Kang W, Bae Y, Kim S, Yoo D, et al.. Escherichia coli hns and methylglyoxal link gut microbial metabolism to host neuronal gene regulation in Parkinson's disease. . 2026. PMID 42878179 · DOI · PMC13679328
- Li P, Wang H, Guo L, Gou X, Chen G, Lin D, et al.. Association between gut microbiota and preeclampsia-eclampsia: a two-sample Mendelian randomization study. BMC Med. 2022. PMID 36380372 · DOI · PMC9667679
- Xu S, Li X, Zhang S, Qi C, Zhang Z, Ma R, et al.. Oxidative stress gene expression, DNA methylation, and gut microbiota interaction trigger Crohn's disease: a multi-omics Mendelian randomization study. BMC Med. 2023. PMID 37170220 · DOI · PMC10173549
- Zhernakova DV, Wang D, Liu L, Andreu-Sánchez S, Zhang Y, Ruiz-Moreno AJ, et al.. Host genetic regulation of human gut microbial structural variation. Nature. 2024. PMID 38172637 · DOI · PMC10808065
- Gunjur A, Shao Y, Rozday T, Klein O, Mu A, Haak BW, et al.. A gut microbial signature for combination immune checkpoint blockade across cancer types. Nat Med. 2024. PMID 38429524 · DOI · PMC10957475
- Zheng Y, Zhang Z, Tang P, Wu Y, Zhang A, Li D, et al.. Probiotics fortify intestinal barrier function: a systematic review and meta-analysis of randomized trials. Front Immunol. 2023. PMID 37168869 · DOI · PMC10165082
- Gao M, Wang J, Liu P, Tu H, Zhang R, Zhang Y, et al.. Gut microbiota composition in depressive disorder: a systematic review, meta-analysis, and meta-regression. Transl Psychiatry. 2023. PMID 38065935 · DOI · PMC10709466
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.