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Cecum

Anatomy and Physiology · NLM MeSH · updated 2026-10-31 · version 1

Citations verified against PubMedNot yet clinician-reviewed10 referencesApproximately 4 min read

The blind sac or outpouching area of the large intestine that is below the entrance of the small intestine.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

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: 4 complete abstracts (662 words), 10 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 blind sac or outpouching area of the large intestine that is below the entrance of the small intestine. It has a worm-like extension, the vermiform appendix.

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: Cecums.

Where it fits in the MeSH classification

Broader topics
Intestine, Large
Narrower topics
Appendix
See also
Cecostomy

Related concepts

  • Large Intestine
  • Small Intestine
  • Appendix

Research landscape

PubMed indexes 22,481 records tagged with the MeSH heading “Cecum” (counts retrieved 2026-10-31). 3,057 of them (13.6%) were published from 2020 onward, and the busiest period so far is through 1999 with 11,221 records.

Reviews account for 822 records (3.7%) and meta-analyses for 63. Randomized controlled trials number 284 (1.3%) 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.

PubMed records by publication periodthrough 1999: 11,221 records; 2000-2009: 3,512 records; 2010-2019: 4,691 records; 2020 onward: 3,057 records11,221through 19993,5122000-20094,6912010-20193,0572020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 199911,221
2000-20093,512
2010-20194,691
2020 onward3,057
Share of records by publication typeReviews: 3.7 percent; Meta-analyses: 0.3 percent; Randomized controlled trials: 1.3 percentReviews3.7% (822)Meta-analyses0.3% (63)Randomized controlled trials1.3% (284)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 22,481 PubMed records
TypeRecordsShare
Reviews8223.7%
Meta-analyses630.3%
Randomized controlled trials2841.3%

Method: PubMed query "Cecum"[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 comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Evaluation of the Molecular Mechanisms of Sepsis Using Proteomics
Miao H, Chen S, Ding R
2021Review article
Design not recorded in structured metadata
43cc by
PMID 34745104 · DOI · PMC8566982
The metabolic footprint of Clostridia and Erysipelotrichia reveals their role in depleting sugar alcohols in the cecum
Tiffany CR, Lee JY, Rogers AWL, Olsan EE, Morales P, Faber F, et al.
2021Research article
Design not recorded in structured metadata
33cc by
PMID 34412707 · DOI · PMC8375055
Epigenetic inactivation of the autophagy-lysosomal system in appendix in Parkinson's disease
Gordevicius J, Li P, Marshall LL, Killinger BA, Lang S, Ensink E, et al.
2021Research article
Design not recorded in structured metadata
30cc by
PMID 34446734 · DOI · PMC8390554
Caecal Epithelium-Derived Thymic Stromal Lymphopoietin is not Required for Protective Immunity Against Whipworm
Lynch CP, Thompson S, Pallott EC, Campbell L, Lee SH, Grencis RK
2026Research article
Design not recorded in structured metadata
0cc by
PMID 42494310 · DOI · PMC13397033

Evaluation of the Molecular Mechanisms of Sepsis Using Proteomics [1]

Review article Miao H, Chen S, Ding R · · 2021 · cited 43 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Sepsis is a complex syndrome promoted by pathogenic and host factors; it is characterized by dysregulated host responses and multiple organ dysfunction, which can lead to death.
Closing excerpt
Although previous reports have summarized proteomics-related data on the diagnosis of sepsis and sepsis-related biomarkers, the present review aims to comprehensively summarize the available literature concerning "sepsis", "proteomics", "cecal ligation and puncture", "lipopolysaccharide", and "post-translational modifications" in relation to proteomics research to provide novel insights into the molecular mechanisms of sepsis.
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)

Sepsis is a complex syndrome promoted by pathogenic and host factors; it is characterized by dysregulated host responses and multiple organ dysfunction, which can lead to death. However, its underlying molecular mechanisms remain unknown. Proteomics, as a biotechnology research area in the post-genomic era, paves the way for large-scale protein characterization. With the rapid development of proteomics technology, various approaches can be used to monitor proteome changes and identify differentially expressed proteins in sepsis, which may help to understand the pathophysiological process of sepsis. Although previous reports have summarized proteomics-related data on the diagnosis of sepsis and sepsis-related biomarkers, the present review aims to comprehensively summarize the available literature concerning "sepsis", "proteomics", "cecal ligation and puncture", "lipopolysaccharide", and "post-translational modifications" in relation to proteomics research to provide novel insights into the molecular mechanisms of sepsis.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34745104 · DOI · PMC8566982

The metabolic footprint of Clostridia and Erysipelotrichia reveals their role in depleting sugar alcohols in the cecum [2]

Research article Tiffany CR, Lee JY, Rogers AWL, Olsan EE, Morales P, Faber F, et al. · · 2021 · cited 33 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
BackgroundThe catabolic activity of the microbiota contributes to health by aiding in nutrition, immune education, and niche protection against pathogens.
Closing excerpt
Video abstract.
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 (226 words)

BackgroundThe catabolic activity of the microbiota contributes to health by aiding in nutrition, immune education, and niche protection against pathogens. However, the nutrients consumed by common taxa within the gut microbiota remain incompletely understood.MethodsHere we combined microbiota profiling with an un-targeted metabolomics approach to determine whether depletion of small metabolites in the cecum of mice correlated with the presence of specific bacterial taxa. Causality was investigated by engrafting germ-free or antibiotic-treated mice with complex or defined microbial communities.ResultsWe noted that a depletion of Clostridia and Erysipelotrichia from the gut microbiota triggered by antibiotic treatment was associated with an increase in the cecal concentration of sugar acids and sugar alcohols (polyols). Notably, when we inoculated germ-free mice with a defined microbial community of 14 Clostridia and 3 Erysipelotrichia isolates, we observed the inverse, with a marked decrease in the concentrations of sugar acids and polyols in cecal contents. The carbohydrate footprint produced by the defined microbial community was similar to that observed in gnotobiotic mice receiving a cecal microbiota transplant from conventional mice. Supplementation with sorbitol, a polyol used as artificial sweetener, increased cecal sorbitol concentrations in antibiotic-treated mice, which was abrogated after inoculation with a Clostridia isolate able to grow on sorbitol in vitro.ConclusionsWe conclude that consumption of sugar alcohols by Clostridia and Erysipelotrichia species depletes these metabolites from the intestinal lumen during homeostasis. Video abstract.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34412707 · DOI · PMC8375055

Epigenetic inactivation of the autophagy-lysosomal system in appendix in Parkinson's disease [3]

Research article Gordevicius J, Li P, Marshall LL, Killinger BA, Lang S, Ensink E, et al. · · 2021 · cited 30 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
The gastrointestinal tract may be a site of origin for α-synuclein pathology in idiopathic Parkinson's disease (PD).
Closing excerpt
Our work identifies epigenetic dysregulation of the ALP which may suggest a potential mechanism for accumulation of α-synuclein pathology in idiopathic PD.
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 (151 words)

The gastrointestinal tract may be a site of origin for α-synuclein pathology in idiopathic Parkinson's disease (PD). Disruption of the autophagy-lysosome pathway (ALP) may contribute to α-synuclein aggregation. Here we examined epigenetic alterations in the ALP in the appendix by deep sequencing DNA methylation at 521 ALP genes. We identified aberrant methylation at 928 cytosines affecting 326 ALP genes in the appendix of individuals with PD and widespread hypermethylation that is also seen in the brain of individuals with PD. In mice, we find that DNA methylation changes at ALP genes induced by chronic gut inflammation are greatly exacerbated by α-synuclein pathology. DNA methylation changes at ALP genes induced by synucleinopathy are associated with the ALP abnormalities observed in the appendix of individuals with PD specifically involving lysosomal genes. Our work identifies epigenetic dysregulation of the ALP which may suggest a potential mechanism for accumulation of α-synuclein pathology in idiopathic PD.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34446734 · DOI · PMC8390554

Caecal Epithelium-Derived Thymic Stromal Lymphopoietin is not Required for Protective Immunity Against Whipworm [4]

Research article Lynch CP, Thompson S, Pallott EC, Campbell L, Lee SH, Grencis RK · · 2026

Abstract reading summary — source excerpts
Opening excerpt
Recent research examining classical type two alarmin TSLP has uncovered non-epithelial cellular sources of the cytokine in various murine challenges.
Closing excerpt
These data build on previous work to raise important questions regarding the interaction of TSLP with immunity broadly, as well as the conditions for the production of immunity to intestinal helminths.
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 (150 words)

Recent research examining classical type two alarmin TSLP has uncovered non-epithelial cellular sources of the cytokine in various murine challenges. Trichuris muris is a key model of type two immunity in the intestine, with expulsion being TSLP-dependent. Previous research has indicated epithelial production of TSLP in the caecum, but its production during infection has not been characterised in detail. Here, conditional knockout of Tslp expression in caecal epithelial cells was shown not to impact parasite expulsion, but, surprisingly, neutralisation of TSLP from days 15 to 25 post-infection produced full susceptibility. qPCR and transcript-based imaging were used to demonstrate that caecal epithelium is a poor source of Tslp, and non-epithelial Tslp expression is observed during Trichuris infection in EpCAM-negative cells. These data build on previous work to raise important questions regarding the interaction of TSLP with immunity broadly, as well as the conditions for the production of immunity to intestinal helminths.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42494310 · DOI · PMC13397033

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 Cecal ligation and puncture: the gold standard model for polymicrobial sepsis? [5]
    Dejager L, Pinheiro I, Dejonckheere E, Libert C · Trends Microbiol · 2011 · cited 598 times (Europe PMC)
  • Research article Cecal ligation and puncture [6]
    Hubbard WJ, Choudhry M, Schwacha MG, Kerby JD, Rue LW, Bland KI, et al. · Shock · 2005 · cited 560 times (Europe PMC)
  • Research article Biofilms in the large bowel suggest an apparent function of the human vermiform appendix [7]
    Randal Bollinger R, Barbas AS, Bush EL, Lin SS, Parker W · J Theor Biol · 2007 · cited 217 times (Europe PMC)
  • Research article Primary neoplasms of the appendix: radiologic spectrum of disease with pathologic correlation [8]
    Pickhardt PJ, Levy AD, Rohrmann CA, Kende AI · Radiographics · 2003 · cited 203 times (Europe PMC)
  • Research article Is bile acid a determinant of the gut microbiota on a high-fat diet? [9]
    Yokota A, Fukiya S, Islam KB, Ooka T, Ogura Y, Hayashi T, et al. · Gut Microbes · 2012 · cited 156 times (Europe PMC)
  • Research article The immunology of the vermiform appendix: a review of the literature [10]
    Kooij IA, Sahami S, Meijer SL, Buskens CJ, Te Velde AA · Clin Exp Immunol · 2016 · cited 140 times (Europe PMC)

References

  1. Miao H, Chen S, Ding R. Evaluation of the Molecular Mechanisms of Sepsis Using Proteomics. . 2021. PMID 34745104 · DOI · PMC8566982
  2. Tiffany CR, Lee JY, Rogers AWL, Olsan EE, Morales P, Faber F, et al.. The metabolic footprint of Clostridia and Erysipelotrichia reveals their role in depleting sugar alcohols in the cecum. . 2021. PMID 34412707 · DOI · PMC8375055
  3. Gordevicius J, Li P, Marshall LL, Killinger BA, Lang S, Ensink E, et al.. Epigenetic inactivation of the autophagy-lysosomal system in appendix in Parkinson's disease. . 2021. PMID 34446734 · DOI · PMC8390554
  4. Lynch CP, Thompson S, Pallott EC, Campbell L, Lee SH, Grencis RK. Caecal Epithelium-Derived Thymic Stromal Lymphopoietin is not Required for Protective Immunity Against Whipworm. . 2026. PMID 42494310 · DOI · PMC13397033
  5. Dejager L, Pinheiro I, Dejonckheere E, Libert C. Cecal ligation and puncture: the gold standard model for polymicrobial sepsis?. Trends Microbiol. 2011. PMID 21296575 · DOI
  6. Hubbard WJ, Choudhry M, Schwacha MG, Kerby JD, Rue LW, Bland KI, et al.. Cecal ligation and puncture. Shock. 2005. PMID 16374373 · DOI
  7. Randal Bollinger R, Barbas AS, Bush EL, Lin SS, Parker W. Biofilms in the large bowel suggest an apparent function of the human vermiform appendix. J Theor Biol. 2007. PMID 17936308 · DOI
  8. Pickhardt PJ, Levy AD, Rohrmann CA, Kende AI. Primary neoplasms of the appendix: radiologic spectrum of disease with pathologic correlation. Radiographics. 2003. PMID 12740466 · DOI
  9. Yokota A, Fukiya S, Islam KB, Ooka T, Ogura Y, Hayashi T, et al.. Is bile acid a determinant of the gut microbiota on a high-fat diet?. Gut Microbes. 2012. PMID 22825495 · DOI
  10. Kooij IA, Sahami S, Meijer SL, Buskens CJ, Te Velde AA. The immunology of the vermiform appendix: a review of the literature. Clin Exp Immunol. 2016. PMID 27271818 · 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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At a glance

22,481
PubMed records on this heading
14%
published since 2020
822
review articles
284
randomized trials
10
verified references below

Counts come from PubMed on 2026-10-31; they show how much has been written, not how strong the evidence is.

Related topics See all →

  • IleumAnatomy and Physiology
  • ColonAnatomy and Physiology
  • JejunumAnatomy and Physiology
  • RectumAnatomy and Physiology
  • Anal CanalAnatomy and Physiology

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