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 (812 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
Chronic, non-specific inflammation of the gastrointestinal tract. Etiology may be genetic or environmental. This term includes crohn disease and ulcerative colitis.
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: Inflammatory Bowel Disease; Bowel Diseases, Inflammatory.
Where it fits in the MeSH classification
- Broader topics
- Gastroenteritis; Intestinal Diseases
- Narrower topics
- Colitis, Ulcerative; Crohn Disease
Related concepts
- Gastrointestinal Tract
- Crohn Disease
- Ulcerative Colitis
Research landscape
PubMed indexes 113,051 records tagged with the MeSH heading “Inflammatory Bowel Diseases” (counts retrieved 2026-11-04). 32,286 of them (28.6%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 33,130 records.
Reviews account for 21,855 records (19.3%) and meta-analyses for 2,018. Randomized controlled trials number 2,553 (2.3%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 28,476 |
| 2000-2009 | 19,159 |
| 2010-2019 | 33,130 |
| 2020 onward | 32,286 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 21,855 | 19.3% |
| Meta-analyses | 2,018 | 1.8% |
| Randomized controlled trials | 2,553 | 2.3% |
Method: PubMed query "Inflammatory Bowel Diseases"[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 |
|---|---|---|---|---|
| Concerted changes in the pediatric single-cell intestinal ecosystem before and after anti-TNF blockade | 2026 | Research article Design not recorded in structured metadata | 10 | cc by PMID 42678060 · DOI · PMC13533482 |
| Corticosteroid-sparing effects of risankizumab versus ustekinumab in patients with moderately to severely active Crohn's disease: post hoc results from the phase 3b SEQUENCE trial | 2026 | Randomized controlled trial Design not recorded in structured metadata | 2 | cc by PMID 42479626 · DOI · PMC13387155 |
| Apoptosis-related genes bridge inflammatory bowel disease and osteoporosis: A bioinformatic analysis | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42585215 · DOI · PMC13465802 |
Concerted changes in the pediatric single-cell intestinal ecosystem before and after anti-TNF blockade [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Crohn's disease is an inflammatory bowel disease (IBD) commonly treated through anti-TNF blockade.
- Closing excerpt
- Our study jointly leverages a treatment-naive cohort, high-resolution principled scRNA-seq data analysis, and clinical outcomes to understand which baseline cell states may predict Crohn's disease trajectory.
- 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 (273 words)
Crohn's disease is an inflammatory bowel disease (IBD) commonly treated through anti-TNF blockade. However, most patients still relapse and inevitably progress. Comprehensive single-cell RNA-sequencing (scRNA-seq) atlases have largely sampled patients with established treatment-refractory IBD, limiting our understanding of which cell types, subsets, and states at diagnosis anticipate disease severity and response to treatment. Here, through combining clinical, flow cytometry, histology, and scRNA-seq methods, we profile diagnostic human biopsies from the terminal ileum of treatment-naive pediatric patients with Crohn's disease (pediCD; n = 14), matched repeat biopsies (pediCD-treated; n = 8) and from non-inflamed pediatric controls with functional gastrointestinal disorders (FGIDs; n = 13). To resolve and annotate epithelial, stromal, and immune cell states among the 201,883 baseline single-cell transcriptomes, we develop a principled and unbiased tiered clustering approach, ARBOL. Through flow cytometry and scRNA-seq, we observe that treatment-naive pediCD and FGID have similar broad cell type composition. However, through high-resolution scRNA-seq analysis and microscopy, we identify significant differences in cell subsets and states that arise during pediCD relative to FGID. By closely linking our scRNA-seq analysis with clinical meta-data, we resolve a vector of T cell, innate lymphocyte, myeloid, and epithelial cell states in treatment-naive pediCD (pediCD-TIME) samples, which can distinguish patients along the trajectory of disease severity and anti-TNF response. By using ARBOL with integration, we position repeat on-treatment biopsies from our patients between treatment-naive pediCD and on-treatment adult CD. We identify that anti-TNF treatment pushes the pediatric cellular ecosystem toward an adult, more treatment-refractory state. Our study jointly leverages a treatment-naive cohort, high-resolution principled scRNA-seq data analysis, and clinical outcomes to understand which baseline cell states may predict Crohn's disease trajectory.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42678060 · DOI · PMC13533482
Corticosteroid-sparing effects of risankizumab versus ustekinumab in patients with moderately to severely active Crohn's disease: post hoc results from the phase 3b SEQUENCE trial [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundThis post hoc analysis evaluated the corticosteroid-sparing effects of risankizumab (RZB) versus ustekinumab (UST) in patients with moderate to severe Crohn's disease (CD) with prior inadequate response or intolerance to ≥ 1 anti-tumor necrosis factor (TNF) therapy.
- Closing excerpt
- Clinical trial registration numberNCT04524611.
- 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 (261 words)
BackgroundThis post hoc analysis evaluated the corticosteroid-sparing effects of risankizumab (RZB) versus ustekinumab (UST) in patients with moderate to severe Crohn's disease (CD) with prior inadequate response or intolerance to ≥ 1 anti-tumor necrosis factor (TNF) therapy.MethodsSEQUENCE (NCT04524611) was an open-label, multicenter, randomized, efficacy assessment-blinded study. Patients were randomized 1:1 to receive RZB (intravenous [IV] 600 mg induction dose at weeks 0, 4, and 8, then a subcutaneous [SC] 360 mg maintenance dose every 8 weeks [Q8w] starting at week 12) or UST (single weight-based IV induction dose, then a SC 90 mg maintenance dose Q8w starting at week 8) up to week 48. Patients tapered corticosteroids beginning at week 2. Achievement of clinical, endoscopic, and quality of life outcomes without concomitant use of steroids ("corticosteroid-free") and safety were assessed.ResultsIn patients taking corticosteroids at baseline, response rate differences by the week 24 and 48 timepoints with RZB versus UST were 10.5% and 25.4% (P ≤ .01) for corticosteroid-free clinical remission per CD activity index and 20.4% (P ≤ .001) and 29.2% (P ≤ .01) per stool frequency/abdominal pain score, and 23.0% and 20.2% (both P ≤ .01) for corticosteroid-free endoscopic remission. Similar results were also observed for additional corticosteroid-free endpoints, including endoscopic, composite (clinical + endoscopic), and quality of life outcomes. Numerically higher exposure-adjusted event rates of serious infections and hypersensitivity with RZB and UST were observed with corticosteroid use.ConclusionIn patients with CD refractory to anti-TNF therapy, higher rates of corticosteroid-free clinical, endoscopic, and quality of life outcomes were achieved with RZB versus UST. Both treatments were well-tolerated.Clinical trial registration numberNCT04524611.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42479626 · DOI · PMC13387155
Apoptosis-related genes bridge inflammatory bowel disease and osteoporosis: A bioinformatic analysis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundInflammatory bowel disease (IBD) and osteoporosis (OP) often co-occur, with IBD accelerating OP onset, though the underlying mechanisms remain unclear.
- Closing excerpt
- ConclusionsWNT1 and S100A8, which are associated with apoptosis, play critical roles in both inflammatory bowel disease and osteoporosis, providing new potential therapeutic targets and a theoretical basis for clinical diagnosis and treatment.
- 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 (278 words)
BackgroundInflammatory bowel disease (IBD) and osteoporosis (OP) often co-occur, with IBD accelerating OP onset, though the underlying mechanisms remain unclear.MethodsBased on gene expression data from the GEO database, differential expression analysis was performed using the limma package to identify genes dysregulated in both IBD and OP. Weighted Gene Co-expression Network Analysis (WGCNA) was employed to explore the associations between genes and phenotypes. Candidate genes were obtained by intersecting differentially expressed genes with key WGCNA modules, followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. To further focus on apoptosis-related mechanisms, the candidate genes were intersected with an apoptosis-related gene set and refined using lasso regression. Core genes were identified through differential expression validation and receiver operating characteristic curve analysis. Subsequently, their potential functions and regulatory networks were explored via multidimensional analysis, gene set enrichment analysis, and Pearson correlation analysis.ResultsWNT1 and S100A8 are closely associated with the progression of both inflammatory bowel disease and osteoporosis. Gene Set Enrichment Analysis revealed that WNT1 is primarily enriched in cell cycle checkpoint signaling, chromosome organization, neuroactive ligand signaling, and neuroactive ligand-receptor interaction. In contrast, S100A8 is mainly enriched in adaptive immune response, adaptive immune response based on somatic recombination of immune receptors built from immunoglobulin superfamily, inflammatory bowel disease, and leishmaniasis. Pearson correlation analysis showed that WNT1 is correlated with TSPAN32, POU3F3, NXPH3, EGFL7, LHX3, TNNI2, HMX1, FAM3A, IBTK, and ZNF747, while S100A8 is correlated with MMP3, SLC6A14, MMP10, S100A9, AQP9, S100A12, CXCL6, CXCR1, SLC38A4, and NCF2.ConclusionsWNT1 and S100A8, which are associated with apoptosis, play critical roles in both inflammatory bowel disease and osteoporosis, providing new potential therapeutic targets and a theoretical basis for clinical diagnosis and treatment.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42585215 · DOI · PMC13465802
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 Food Processing and Risk of Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis [4]
- Research article Oxidative stress-related biomarkers as promising indicators of inflammatory bowel disease activity: A systematic review and meta-analysis [5]
- Research article Comparative Efficacy of Biologics and Small Molecule in Ulcerative Colitis: A Systematic Review and Network Meta-analysis [6]
- Research article Comparative Efficacy of Advanced Therapies for Management of Moderate-to-Severe Ulcerative Colitis: 2024 American Gastroenterological Association Evidence Synthesis [7]
- Research article The bidirectional risk of inflammatory bowel disease and anxiety or depression: A systematic review and meta-analysis [8]
- Research article Diagnostic Accuracy of Intestinal Ultrasound in the Detection of Intra-Abdominal Complications in Crohn's Disease: A Systematic Review and Meta-Analysis [9]
Full-text reviews on EvidenceLib
Open-access review articles about this topic, reproduced in full with authors, licence and references.
Ear, Nose, and Throat Manifestations in Inflammatory Bowel Diseases: A Systematic Review of the Clinical Spectrum
Eleni Litsou, Georgios Psychogios, Maria Saridi et al. · Medicina 2026 · CC BY 4.0
Phytochemicals and Regulation of NF-kB in Inflammatory Bowel Diseases: An Overview of In Vitro and In Vivo Effects
Lucas Fornari Laurindo, Ana Rita de Oliveira dos Santos, Antonelly Cassio Alves de Carvalho et al. · Metabolites 2023 · CC BY 4.0
Pathophysiology of Inflammatory Bowel Disease: Innate Immune System
Angela Saez, Beatriz Herrero-Fernandez, Raquel Gomez-Bris et al. · International Journal of Molecular Sciences 2023 · CC BY 4.0
Neuroinflammation as an etiological trigger for depression comorbid with inflammatory bowel disease
Colin F. Craig, Rhiannon T. Filippone, Rhian Stavely et al. · Journal of Neuroinflammation 2022 · CC BY 4.0
Clinical management of the most common extra-intestinal manifestations in patients with inflammatory bowel disease focused on the joints, skin and eyes
Fenna M Jansen, Stephan R Vavricka, Alfons A den Broeder et al. · United European Gastroenterology Journal 2020 · CC BY 4.0
References
- Zheng HB, Doran BA, Kimler K, Yu A, Tkachev V, Niederlova V, et al.. Concerted changes in the pediatric single-cell intestinal ecosystem before and after anti-TNF blockade. . 2026. PMID 42678060 · DOI · PMC13533482
- Raine T, Danese S, Schreiber S, Gao X, Hanauer S, Torres J, et al.. Corticosteroid-sparing effects of risankizumab versus ustekinumab in patients with moderately to severely active Crohn's disease: post hoc results from the phase 3b SEQUENCE trial. . 2026. PMID 42479626 · DOI · PMC13387155
- Su Y, Luo X, Xu H. Apoptosis-related genes bridge inflammatory bowel disease and osteoporosis: A bioinformatic analysis. . 2026. PMID 42585215 · DOI · PMC13465802
- Narula N, Chang NH, Mohammad D, Wong ECL, Ananthakrishnan AN, Chan SSM, et al.. Food Processing and Risk of Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis. Clin Gastroenterol Hepatol. 2023. PMID 36731590 · DOI
- Tratenšek A, Locatelli I, Grabnar I, Drobne D, Vovk T. Oxidative stress-related biomarkers as promising indicators of inflammatory bowel disease activity: A systematic review and meta-analysis. Redox Biol. 2024. PMID 39368456 · DOI · PMC11490685
- Shehab M, Alrashed F, Alsayegh A, Aldallal U, Ma C, Narula N, et al.. Comparative Efficacy of Biologics and Small Molecule in Ulcerative Colitis: A Systematic Review and Network Meta-analysis. Clin Gastroenterol Hepatol. 2025. PMID 39182898 · DOI
- Ananthakrishnan AN, Murad MH, Scott FI, Agrawal M, Haydek JP, Limketkai BN, et al.. Comparative Efficacy of Advanced Therapies for Management of Moderate-to-Severe Ulcerative Colitis: 2024 American Gastroenterological Association Evidence Synthesis. Gastroenterology. 2024. PMID 39425738 · DOI · PMC12148344
- Bisgaard TH, Allin KH, Elmahdi R, Jess T. The bidirectional risk of inflammatory bowel disease and anxiety or depression: A systematic review and meta-analysis. Gen Hosp Psychiatry. 2023. PMID 37172544 · DOI
- Pruijt MJ, de Voogd FAE, Montazeri NSM, van Etten-Jamaludin FS, D'Haens GR, Gecse KB. Diagnostic Accuracy of Intestinal Ultrasound in the Detection of Intra-Abdominal Complications in Crohn's Disease: A Systematic Review and Meta-Analysis. J Crohns Colitis. 2024. PMID 38173288 · DOI · PMC11147796
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.