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 (668 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
Inflammation of the colon section of the large intestine (intestine, large), usually with symptoms such as diarrhea (often with blood and mucus), abdominal pain, and fever.
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: Colitides.
Where it fits in the MeSH classification
- Broader topics
- Gastroenteritis; Colonic Diseases
- Narrower topics
- Colitis, Ischemic; Colitis, Microscopic; Colitis, Ulcerative; Proctocolitis
Related concepts
- Colon
- Intestines
- Large
- Diarrhea
- Abdominal Pain
- Fever
Research landscape
PubMed indexes 72,889 records tagged with the MeSH heading “Colitis” (counts retrieved 2026-11-04). 20,120 of them (27.6%) were published from 2020 onward, and the busiest period so far is through 1999 with 22,518 records.
Reviews account for 8,422 records (11.6%) and meta-analyses for 931. Randomized controlled trials number 1,344 (1.8%) 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 | 22,518 |
| 2000-2009 | 11,073 |
| 2010-2019 | 19,178 |
| 2020 onward | 20,120 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 8,422 | 11.6% |
| Meta-analyses | 931 | 1.3% |
| Randomized controlled trials | 1,344 | 1.8% |
Method: PubMed query "Colitis"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in digestive system and liver
Gut and liver research ranges from laboratory studies of the microbiome to large trials of drugs and surgery. Symptoms such as pain, reflux or bowel change are reported by patients and overlap between conditions, and diet and microbiome studies are mostly observational. Check whether the study measured symptoms, tissue findings or long-term outcomes, how the diagnosis was made and how long people were followed. Nothing here replaces advice from a qualified clinician.
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 |
|---|---|---|---|---|
| Single-cell spatial transcriptomics of formalin-fixed, paraffin-embedded biopsies reveals colitis-associated cell networks | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 42262875 · DOI · PMC13367960 |
| Context-Dependent Epithelial and Immune Programs Shape Intestinal Resilience or Vulnerability Following Prior Colitis | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42269772 · DOI · PMC13400666 |
| A context-dependent METTL1-m7G-SLC7A11 axis links metabolic stress to epithelial fate in ulcerative colitis | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42212324 · DOI · PMC13215248 |
Single-cell spatial transcriptomics of formalin-fixed, paraffin-embedded biopsies reveals colitis-associated cell networks [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Imaging-based, single-cell, spatial transcriptomics (iSCST) of FFPE tissue enables comprehensive analysis of archived specimens while preserving spatial context, critical to an understanding of ulcerative colitis (UC) pathology.
- Closing excerpt
- This iSCST framework provides a powerful approach for analyzing FFPE tissues, offering insights into colitis-associated cellular networks and identifying biomarkers to enhance patient risk stratification in routine clinical workflows.
- 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 (188 words)
Imaging-based, single-cell, spatial transcriptomics (iSCST) of FFPE tissue enables comprehensive analysis of archived specimens while preserving spatial context, critical to an understanding of ulcerative colitis (UC) pathology. Here, we deployed a robust framework for applying iSCST to clinical FFPE mucosal biopsies from patients with UC or immune checkpoint inhibitor-induced colitis, as well as patients serving as healthy controls. iSCST using custom Xenium gene panels enabled precise detection of diverse cell subsets and disease-specific genes. We mapped transcriptionally distinct fibroblast subsets within mucosal niches, including inflammation-associated fibroblasts (IAFs), and identified colitis-specific neighborhoods formed by IAFs, monocytes, and neutrophils. Transcriptional signatures and spatial neighborhoods uncovered through iSCST were associated with vedolizumab (VDZ) response, with nonresponders exhibiting either an innate IAF-monocyte-neutrophil signature or adaptive gut-associated lymphoid tissue signature, while responders showed enrichment of an epithelial cellular neighborhood. These signatures were validated in an internal and an external dataset, supporting the existence of 2 distinct archetypes of treatment resistance to VDZ in UC. This iSCST framework provides a powerful approach for analyzing FFPE tissues, offering insights into colitis-associated cellular networks and identifying biomarkers to enhance patient risk stratification in routine clinical workflows.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42262875 · DOI · PMC13367960
Context-Dependent Epithelial and Immune Programs Shape Intestinal Resilience or Vulnerability Following Prior Colitis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Background & aimsPrior intestinal inflammation can leave durable immune and epithelial alterations, yet how these changes influence responses to subsequent injury remains unclear.
- Closing excerpt
- These findings highlight how inflammatory history influences long-term intestinal resilience or vulnerability.
- 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 (280 words)
Background & aimsPrior intestinal inflammation can leave durable immune and epithelial alterations, yet how these changes influence responses to subsequent injury remains unclear. Infectious and sterile colitis share core features, including barrier disruption and cytokine secretion. We therefore investigated whether the nature of the initial inflammatory event shapes protection or susceptibility during later intestinal insult.MethodsWe used reciprocal mouse models of Citrobacter rodentium infection and dextran sodium sulphate-induced colitis to define how prior infectious vs sterile colitis shapes secondary disease. Barrier integrity, immune cell populations, cytokine production, and susceptibility to wild-type and C rodentium mutants that cause limited epithelial barrier disruption were assessed.ResultsMice recovered from C rodentium infection were protected against dextran sodium sulphate-induced colitis, displaying reduced weight loss, preserved epithelial architecture, and lower inflammatory pathology. This protection required type III secretion system effector-mediated epithelial injury during primary infection and was associated with sustained interleukin17A signaling, which contributed to the protective phenotype. In contrast, mice recovered from dextran sodium sulphate-induced colitis exhibited persistent epithelial barrier defects, chronic colonic neutrophilia, and heightened susceptibility to C rodentium infection despite elevated interleukin17A. Infection with C rodentium mutants that cause minimal epithelial damage still resulted in severe disease in dextran sodium sulphate-experienced mice, indicating that unresolved epithelial barrier dysfunction is a major contributor to vulnerability.ConclusionsThe nature of the primary colitis is associated with distinct epithelial and immune programs that persist beyond resolution of inflammation. Infectious colitis is associated with a protective mucosal state where interleukin17A is a key contributor in a broader protective response, whereas sterile colitis is associated with persistent epithelial barrier dysfunction that is associated with increased susceptibility to subsequent infection. These findings highlight how inflammatory history influences long-term intestinal resilience or vulnerability.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42269772 · DOI · PMC13400666
A context-dependent METTL1-m7G-SLC7A11 axis links metabolic stress to epithelial fate in ulcerative colitis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Ulcerative colitis (UC) is characterized by chronic intestinal inflammation accompanied by epithelial barrier dysfunction and profound metabolic stress; however, how metabolic cues are integrated to determine epithelial cell fate remains incompletely understood.
- Closing excerpt
- Collectively, these findings establish the METTL1-m7G-SLC7A11 axis as a metabolic rheostat that integrates inflammatory cues and nutrient availability to determine epithelial cell fate in UC, highlighting the importance of stage- and context-specific therapeutic strategies.
- 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 (200 words)
Ulcerative colitis (UC) is characterized by chronic intestinal inflammation accompanied by epithelial barrier dysfunction and profound metabolic stress; however, how metabolic cues are integrated to determine epithelial cell fate remains incompletely understood. Here, we identify a context-dependent METTL1-m7G-SLC7A11 regulatory axis that links metabolic stress to intestinal epithelial outcomes during UC progression. By integrating analyses of human UC tissues, DSS-induced acute and chronic colitis mouse models, and mechanistic in vitro experiments, we demonstrate that METTL1 enhances N7-methylguanosine (m7G) modification of SLC7A11 mRNA, thereby stabilizing the transcript and sustaining SLC7A11 expression in inflammatory settings. Functionally, SLC7A11 exhibits glucose-dependent dual effects. Under glucose-replete conditions, SLC7A11 supports cystine uptake, glutathione synthesis, and redox homeostasis, protecting epithelial integrity and limiting inflammation. In contrast, under glucose deprivation-a characteristic feature of inflamed UC mucosa-persistent SLC7A11 activation induces disulfide stress, cytoskeletal collapse, and disulfidptosis-associated epithelial injury. In vivo, inhibition of the METTL1/m7G/SLC7A11 axis exacerbates chronic DSS-induced colitis but alleviates acute DSS-induced colitis, revealing a switch from adaptive to maladaptive signaling with escalating metabolic stress. Collectively, these findings establish the METTL1-m7G-SLC7A11 axis as a metabolic rheostat that integrates inflammatory cues and nutrient availability to determine epithelial cell fate in UC, highlighting the importance of stage- and context-specific therapeutic strategies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42212324 · DOI · PMC13215248
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 Environmental Risk Factors for Inflammatory Bowel Diseases: An Umbrella Review of Meta-analyses [4]
- Research article Long-term dietary patterns are associated with pro-inflammatory and anti-inflammatory features of the gut microbiome [5]
- Research article First- and Second-Line Pharmacotherapies for Patients With Moderate to Severely Active Ulcerative Colitis: An Updated Network Meta-Analysis [6]
- Research article Efficacy and safety of biologics and small molecule drugs for patients with moderate-to-severe ulcerative colitis: a systematic review and network meta-analysis [7]
- Research article Contemporary Risk of Surgery in Patients With Ulcerative Colitis and Crohn's Disease: A Meta-Analysis of Population-Based Cohorts [8]
- Research article Global Hospitalization Trends for Crohn's Disease and Ulcerative Colitis in the 21st Century: A Systematic Review With Temporal Analyses [9]
Full-text reviews on EvidenceLib
Open-access review articles about this topic, reproduced in full with authors, licence and references.
Anti-inflammatory and antioxidant activity of astragalus polysaccharide in ulcerative colitis: A systematic review and meta-analysis of animal studies
Heng-Chang Hu, Wei Zhang, Pei-Yu Xiong et al. · Frontiers in Pharmacology 2022 · CC BY 4.0
Effects of Low and High FODMAP Diets on Human Gastrointestinal Microbiota Composition in Adults with Intestinal Diseases: A Systematic Review
Doris Vandeputte, Marie Joossens · Microorganisms 2020 · CC BY 4.0
References
- Mennillo E, Lotstein ML, Lee G, Hou JH, Johri V, Leet DE, et al.. Single-cell spatial transcriptomics of formalin-fixed, paraffin-embedded biopsies reveals colitis-associated cell networks. . 2026. PMID 42262875 · DOI · PMC13367960
- Biswas P, Mishra V, Sanchez-Garrido J, Frankel G. Context-Dependent Epithelial and Immune Programs Shape Intestinal Resilience or Vulnerability Following Prior Colitis. . 2026. PMID 42269772 · DOI · PMC13400666
- Yang L, Sun Q, Jiang Z, Yao B, Yang C, Liu G, et al.. A context-dependent METTL1-m7G-SLC7A11 axis links metabolic stress to epithelial fate in ulcerative colitis. . 2026. PMID 42212324 · DOI · PMC13215248
- Piovani D, Danese S, Peyrin-Biroulet L, Nikolopoulos GK, Lytras T, Bonovas S. Environmental Risk Factors for Inflammatory Bowel Diseases: An Umbrella Review of Meta-analyses. Gastroenterology. 2019. PMID 31014995 · DOI
- Bolte LA, Vich Vila A, Imhann F, Collij V, Gacesa R, Peters V, et al.. Long-term dietary patterns are associated with pro-inflammatory and anti-inflammatory features of the gut microbiome. Gut. 2021. PMID 33811041 · DOI · PMC8223641
- Singh S, Murad MH, Fumery M, Dulai PS, Sandborn WJ. First- and Second-Line Pharmacotherapies for Patients With Moderate to Severely Active Ulcerative Colitis: An Updated Network Meta-Analysis. Clin Gastroenterol Hepatol. 2020. PMID 31945470 · DOI · PMC8022894
- Lasa JS, Olivera PA, Danese S, Peyrin-Biroulet L. Efficacy and safety of biologics and small molecule drugs for patients with moderate-to-severe ulcerative colitis: a systematic review and network meta-analysis. Lancet Gastroenterol Hepatol. 2022. PMID 34856198 · DOI
- Tsai L, Ma C, Dulai PS, Prokop LJ, Eisenstein S, Ramamoorthy SL, et al.. Contemporary Risk of Surgery in Patients With Ulcerative Colitis and Crohn's Disease: A Meta-Analysis of Population-Based Cohorts. Clin Gastroenterol Hepatol. 2021. PMID 33127595 · DOI · PMC8934200
- Buie MJ, Quan J, Windsor JW, Coward S, Hansen TM, King JA, et al.. Global Hospitalization Trends for Crohn's Disease and Ulcerative Colitis in the 21st Century: A Systematic Review With Temporal Analyses. Clin Gastroenterol Hepatol. 2023. PMID 35863682 · 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 2026-11-04; 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.