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 (571 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 section of the alimentary canal from the stomach to the anal canal. It includes the large intestine and small intestine.
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: Intestine.
Where it fits in the MeSH classification
- Broader topics
- Gastrointestinal Tract
- Narrower topics
- Intestinal Mucosa; Intestine, Large; Intestine, Small
- See also
- Enterostomy; Gastroenterostomy
Related concepts
- Stomach
- Anal Canal
- Large Intestine
- Small Intestine
Research landscape
PubMed indexes 442,485 records tagged with the MeSH heading “Intestines” (counts retrieved 2026-10-31). 54,259 of them (12.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 222,223 records.
Reviews account for 35,252 records (8.0%) and meta-analyses for 1,514. Randomized controlled trials number 6,759 (1.5%) 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 | 222,223 |
| 2000-2009 | 72,218 |
| 2010-2019 | 93,785 |
| 2020 onward | 54,259 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 35,252 | 8.0% |
| Meta-analyses | 1,514 | 0.3% |
| Randomized controlled trials | 6,759 | 1.5% |
Method: PubMed query "Intestines"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
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 |
|---|---|---|---|---|
| Golgi organization regulates stem cell function in the small intestine | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42532997 · DOI · PMC13424321 |
| Mucin O-glycan degradation by GH101 underpins mucosal persistence of Bifidobacterium bifidum PRL2010 | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42470485 · DOI · PMC13612775 |
| Intestinal Epithelial MHC-II at the Interface of Microbiota, Immunity, and Inflammation | 2026 | Review article Design not recorded in structured metadata | 1 | cc by PMID 42653276 · DOI · PMC13513351 |
Golgi organization regulates stem cell function in the small intestine [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Cell-to-cell signaling between niche and stem cells regulates tissue renewal.
- Closing excerpt
- Our results reveal a stem cell-specific Golgi complex configuration that facilitates efficient niche signal reception and tissue renewal, which is compromised in the aged epithelium.
- 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 (174 words)
Cell-to-cell signaling between niche and stem cells regulates tissue renewal. While the identity of many mediating factors is known, it is largely unknown whether stem cells optimize their receptiveness to niche signals according to the niche organization. Here, we show that Lgr5+ small intestinal stem cells (ISCs) regulate the morphology and orientation of their secretory apparatus to match the niche architecture, and to increase transport efficiency of niche signal receptors. ISCs orient their Golgi apparatus laterally towards Paneth cells of the epithelial niche, and divide Golgi into multiple stacks. Stem cells with multiple lateral Golgi transport stem cell receptors with a higher efficiency than cells with one single Golgi. The lateral Golgi orientation and enhanced receptor transport requires A-kinase anchor protein 9 (Akap9), and is necessary for normal renewal capacity. Moreover, reduced Akap9 in aged ISCs renders ISCs insensitive to niche-dependent modulation of Golgi stack number and transport efficiency. Our results reveal a stem cell-specific Golgi complex configuration that facilitates efficient niche signal reception and tissue renewal, which is compromised in the aged epithelium.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42532997 · DOI · PMC13424321
Mucin O-glycan degradation by GH101 underpins mucosal persistence of Bifidobacterium bifidum PRL2010 [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Host-derived mucin O-glycans constitute a key chemical component of the human intestinal niche and are continuously encountered by gut-adapted bifidobacterial cells, thereby playing a pivotal role in host-microbe interactions.
- Closing excerpt
- • These findings reveal a mechanistic connection between mucin glycan metabolism and ecological fitness by mucin-adapted bifidobacterial commensals.
- 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 (262 words)
Host-derived mucin O-glycans constitute a key chemical component of the human intestinal niche and are continuously encountered by gut-adapted bifidobacterial cells, thereby playing a pivotal role in host-microbe interactions. Among these microbes, Bifidobacterium bifidum is one of the most persistent members of the human gut microbiota. Comparative genomic analyses of mucosa-associated strains of this species have revealed a gene conserved across its pangenome, predicted to encode a GH101 glycoside hydrolase involved in mucin degradation. In this study, we performed a molecular characterization of the GH101 enzyme encoded by B. bifidum PRL2010. Insertional mutagenesis of the GH101 gene from the PRL2010 genome resulted in a marked reduction in bacterial adhesion to mucin-secreting epithelial cells, along with a significant growth difference when N-acetyl-galactosamine was provided as the sole carbon source. These findings indicate that GH101 mediates the initial cleavage of O-GalNAc core 1 structures, representing a crucial step for the adhesion to human mucosa. However, this enzyme represents only one component of the broader set of glycosidases required for the complete degradation of host mucins. Overall, our results establish a mechanistic link between metabolic specialization and ecological fitness, providing insights into how mucin-adapted commensals may contribute to interactions with the human gut mucosa. KEY POINTS: • The GH101 glycoside hydrolase of Bifidobacterium bifidum PRL2010 plays a pivotal role in host mucin utilization by initiating the cleavage of O-GalNAc core 1 structures. • Insertional mutant of the GH101 gene impairs both mucosal adhesion and growth on N-acetyl-galactosamine. • These findings reveal a mechanistic connection between mucin glycan metabolism and ecological fitness by mucin-adapted bifidobacterial commensals.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42470485 · DOI · PMC13612775
Intestinal Epithelial MHC-II at the Interface of Microbiota, Immunity, and Inflammation [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Major histocompatibility complex class II (MHC-II) expression by intestinal epithelial cells (IECs) has emerged as a critical mechanism regulating mucosal immune homeostasis at the interface between the intestinal microbiota, epithelial barrier, and immune system.
- Closing excerpt
- This review summarizes current knowledge regarding the molecular regulation, spatial organization, and immunological functions of epithelial MHC-II and discusses its emerging role in host-microbiota interactions, mucosal barrier homeostasis, and intestinal disease.
- 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 (135 words)
Major histocompatibility complex class II (MHC-II) expression by intestinal epithelial cells (IECs) has emerged as a critical mechanism regulating mucosal immune homeostasis at the interface between the intestinal microbiota, epithelial barrier, and immune system. Beyond professional antigen-presenting cells, IEC-intrinsic MHC-II shapes CD4+ T-cell responses, influencing tolerance to commensal microorganisms, immunity to enteric pathogens, and maintenance of barrier integrity. Recent studies have revealed that epithelial MHC-II expression is dynamically regulated by cytokines, the gut microbiota, dietary factors, and microbiota-derived metabolites, linking environmental signals to local adaptive immune responses. Dysregulation of epithelial antigen presentation has been implicated in chronic intestinal inflammation, including inflammatory bowel disease (IBD). This review summarizes current knowledge regarding the molecular regulation, spatial organization, and immunological functions of epithelial MHC-II and discusses its emerging role in host-microbiota interactions, mucosal barrier homeostasis, and intestinal disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42653276 · DOI · PMC13513351
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 Intestinal dysbiosis in preterm infants preceding necrotizing enterocolitis: a systematic review and meta-analysis [4]
- Research article Incremental Benefit of Achieving Endoscopic and Histologic Remission in Patients With Ulcerative Colitis: A Systematic Review and Meta-Analysis [5]
- Research article Intracorporeal versus extracorporeal anastomosis in right hemicolectomy: a systematic review and meta-analysis [6]
- Research article Systematic review with meta-analysis: rifaximin is effective and safe for the treatment of small intestine bacterial overgrowth [7]
- Research article Predictors of inadequate bowel preparation for colonoscopy: a systematic review and meta-analysis [8]
- Research article Bundles Prevent Surgical Site Infections After Colorectal Surgery: Meta-analysis and Systematic Review [9]
References
- Belevich I, Porcile L, Sola-Carvajal A, Grommisch D, Annusvar K, Heinz P, et al.. Golgi organization regulates stem cell function in the small intestine. . 2026. PMID 42532997 · DOI · PMC13424321
- Muscò A, Longhi G, Selleri E, Gennaioli E, Lugli GA, Tarracchini C, et al.. Mucin O-glycan degradation by GH101 underpins mucosal persistence of Bifidobacterium bifidum PRL2010. . 2026. PMID 42470485 · DOI · PMC13612775
- de Oliveira S, Fachi JL. Intestinal Epithelial MHC-II at the Interface of Microbiota, Immunity, and Inflammation. . 2026. PMID 42653276 · DOI · PMC13513351
- Pammi M, Cope J, Tarr PI, Warner BB, Morrow AL, Mai V, et al.. Intestinal dysbiosis in preterm infants preceding necrotizing enterocolitis: a systematic review and meta-analysis. Microbiome. 2017. PMID 28274256 · DOI · PMC5343300
- Yoon H, Jangi S, Dulai PS, Boland BS, Prokop LJ, Jairath V, et al.. Incremental Benefit of Achieving Endoscopic and Histologic Remission in Patients With Ulcerative Colitis: A Systematic Review and Meta-Analysis. Gastroenterology. 2020. PMID 32585306 · DOI · PMC7658293
- van Oostendorp S, Elfrink A, Borstlap W, Schoonmade L, Sietses C, Meijerink J, et al.. Intracorporeal versus extracorporeal anastomosis in right hemicolectomy: a systematic review and meta-analysis. Surg Endosc. 2017. PMID 27287905 · DOI · PMC5216072
- Gatta L, Scarpignato C. Systematic review with meta-analysis: rifaximin is effective and safe for the treatment of small intestine bacterial overgrowth. Aliment Pharmacol Ther. 2017. PMID 28078798 · DOI · PMC5299503
- Mahmood S, Farooqui SM, Madhoun MF. Predictors of inadequate bowel preparation for colonoscopy: a systematic review and meta-analysis. Eur J Gastroenterol Hepatol. 2018. PMID 29847488 · DOI
- Zywot A, Lau CSM, Stephen Fletcher H, Paul S. Bundles Prevent Surgical Site Infections After Colorectal Surgery: Meta-analysis and Systematic Review. J Gastrointest Surg. 2017. PMID 28620749 · DOI
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 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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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.