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 (703 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 space enclosed by the peritoneum. It is divided into two portions, the greater sac and the lesser sac or omental bursa, which lies behind the stomach. The two sacs are connected by the foramen of Winslow, or epiploic foramen.
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: Cavity, Peritoneal; Lesser Sac; Sac, Lesser; Omental Bursa; Bursa, Omental; Greater Sac; Sac, Greater.
Where it fits in the MeSH classification
- Broader topics
- Peritoneum
- See also
- Ascitic Fluid; Laparoscopy
Related concepts
Research landscape
PubMed indexes 9,913 records tagged with the MeSH heading “Peritoneal Cavity” (counts retrieved 2026-10-31). 228 of them (2.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 7,177 records.
Reviews account for 372 records (3.8%) and meta-analyses for 17. Randomized controlled trials number 101 (1.0%) 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 | 7,177 |
| 2000-2009 | 1,410 |
| 2010-2019 | 1,098 |
| 2020 onward | 228 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 372 | 3.8% |
| Meta-analyses | 17 | 0.2% |
| Randomized controlled trials | 101 | 1.0% |
Method: PubMed query "Peritoneal Cavity"[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 |
|---|---|---|---|---|
| Recruited macrophages that colonize the post-inflammatory peritoneal niche convert into functionally divergent resident cells | 2021 | Research article Design not recorded in structured metadata | 136 | cc by PMID 33741914 · DOI · PMC7979918 |
| Activated peritoneal cavity B-1a cells possess regulatory B cell properties | 2014 | Research article Design not recorded in structured metadata | 39 | cc by PMID 24551182 · DOI · PMC3923827 |
| Nanotube action between human mesothelial cells reveals novel aspects of inflammatory responses | 2011 | Research article Design not recorded in structured metadata | 33 | cc by PMID 22216308 · DOI · PMC3246504 |
| Phosphatidylserine phospholipase A1 enables GPR34-dependent immune cell accumulation in the peritoneal cavity | 2024 | Research article Design not recorded in structured metadata | 6 | cc by PMID 39412501 · DOI · PMC11488134 |
Recruited macrophages that colonize the post-inflammatory peritoneal niche convert into functionally divergent resident cells [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Inflammation generally leads to recruitment of monocyte-derived macrophages.
- Closing excerpt
- Hence, rather than being predetermined, the fate of inflammation-elicited peritoneal macrophages seems to be regulated by the environment.
- 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 (144 words)
Inflammation generally leads to recruitment of monocyte-derived macrophages. What regulates the fate of these cells and to what extent they can assume the identity and function of resident macrophages is unclear. Here, we show that macrophages elicited into the peritoneal cavity during mild inflammation persist long-term but are retained in an immature transitory state of differentiation due to the presence of enduring resident macrophages. By contrast, severe inflammation results in ablation of resident macrophages and a protracted phase wherein the cavity is incapable of sustaining a resident phenotype, yet ultimately elicited cells acquire a mature resident identity. These macrophages also have transcriptionally and functionally divergent features that result from inflammation-driven alterations to the peritoneal cavity micro-environment and, to a lesser extent, effects of origin and time-of-residency. Hence, rather than being predetermined, the fate of inflammation-elicited peritoneal macrophages seems to be regulated by the environment.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33741914 · DOI · PMC7979918
Activated peritoneal cavity B-1a cells possess regulatory B cell properties [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Previous studies have suggested that murine peritoneal cavity-derived B-1a cells possess similarities with described regulatory B cell subsets.
- Closing excerpt
- The current paper compares splenic B cells to peritoneal cavity B(-1a) cells in an in vitro activation- and an suppression-assay and concludes that peritoneal cavity B(-1a) cells possess properties that appear similar to splenic autoimmune-suppressive regulatory B cell subsets described in the literature.
- 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 (181 words)
Previous studies have suggested that murine peritoneal cavity-derived B-1a cells possess similarities with described regulatory B cell subsets. The aim of the current study was to examine the potential immunoregulatory function of peritoneal cavity-derived B(-1a) cells. In vitro activation of peritoneal cavity-derived B- and B-1a cells shows that activation of these B cells with anti-CD40 and LPS induces these cells to secrete more IL-10, IL-6 and IgM as compared to splenic B cells. In a suppression assay, CD40/TLR4-activated peritoneal cavity B cells possess regulatory B cell functions as they inhibit the capacity of CD4(+) T cells to produce both tumor necrosis factor-α and interferon-γ. Splenic B cells did not show this, whereas non-activated peritoneal cavity B cells augmented the capacity of CD4(+) T cells to produce tumor necrosis factor-α, while the ability to produce interferon-γ was not altered. The current paper compares splenic B cells to peritoneal cavity B(-1a) cells in an in vitro activation- and an suppression-assay and concludes that peritoneal cavity B(-1a) cells possess properties that appear similar to splenic autoimmune-suppressive regulatory B cell subsets described in the literature.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 24551182 · DOI · PMC3923827
Nanotube action between human mesothelial cells reveals novel aspects of inflammatory responses [3]
Abstract reading summary — source excerpts
- Opening excerpt
- A well-known role of human peritoneal mesothelial cells (HPMCs), the resident cells of the peritoneal cavity, is the generation of an immune response during peritonitis by activation of T-cells via antigen presentation.
- Closing excerpt
- Furthermore, we show that TNF-α induces nanotube formation and demonstrate a strong correlation of NT connectivity in accordance with the cellular cholesterol level and distribution, pointing to a complex involvement of NTs in inflammatory processes with potential impact for clinical 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 (195 words)
A well-known role of human peritoneal mesothelial cells (HPMCs), the resident cells of the peritoneal cavity, is the generation of an immune response during peritonitis by activation of T-cells via antigen presentation. Recent findings have shown that intercellular nanotubes (NTs) mediate functional connectivity between various cell types including immune cells - such as T-cells, natural killer (NK) cells or macrophages - by facilitating a spectrum of long range cell-cell interactions. Although of medical interest, the relevance of NT-related findings for human medical conditions and treatment, e.g. in relation to inflammatory processes, remains elusive, particularly due to a lack of appropriate in vivo data. Here, we show for the first time that primary cultures of patient derived HPMCs are functionally connected via membranous nanotubes. NT formation appears to be actin cytoskeleton dependent, mediated by the action of filopodia. Importantly, significant variances in NT numbers between different donors as a consequence of pathophysiological alterations were observable. Furthermore, we show that TNF-α induces nanotube formation and demonstrate a strong correlation of NT connectivity in accordance with the cellular cholesterol level and distribution, pointing to a complex involvement of NTs in inflammatory processes with potential impact for clinical treatment.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 22216308 · DOI · PMC3246504
Phosphatidylserine phospholipase A1 enables GPR34-dependent immune cell accumulation in the peritoneal cavity [4]
Abstract reading summary — source excerpts
- Opening excerpt
- The peritoneal cavity (PerC) is an important site for immune responses to infection and cancer metastasis.
- Closing excerpt
- These findings provide in vivo evidence that PLA1A produces lysoPS that can regulate GPR34-mediated immune cell accumulation at the omentum.
- 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 peritoneal cavity (PerC) is an important site for immune responses to infection and cancer metastasis. Yet few ligand-receptor axes are known to preferentially govern immune cell accumulation in this compartment. GPR34 is a lysophosphatidylserine (lysoPS)-responsive receptor that frequently harbors gain-of-function mutations in mucosa-associated B cell lymphoma. Here, we set out to test the impact of a GPR34 knock-in (KI) allele in the B-lineage. We report that GPR34 KI promotes the PerC accumulation of plasma cells (PC) and memory B cells (MemB). These KI cells migrate robustly to lysoPS ex vivo, and the KI allele synergizes with a Bcl2 transgene to promote MemB but not PC accumulation. Gene expression and labeling studies reveal that GPR34 KI enhances PerC MemB proliferation. Both KI PC and MemB are specifically enriched at the omentum, a visceral adipose tissue containing fibroblasts that express the lysoPS-generating PLA1A enzyme. Adoptive transfer and chimera experiments revealed that KI PC and MemB maintenance in the PerC is dependent on stromal PLA1A. These findings provide in vivo evidence that PLA1A produces lysoPS that can regulate GPR34-mediated immune cell accumulation at the omentum.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39412501 · DOI · PMC11488134
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 Pharmacokinetic problems in peritoneal drug administration: tissue penetration and surface exposure [5]
- Research article Oxidative stress in the pelvic cavity and its role in the pathogenesis of endometriosis [6]
- Research article ASPECTS OF THE PATHOGENESIS OF VIRUS DISEASES [7]
- Research article Intraperitoneal chemotherapy in advanced gastric cancer. Meta-analysis of randomized trials [8]
- Research article The transport barrier in intraperitoneal therapy [9]
- Research article Clinical problem of intraperitoneal postsurgical adhesion formation following general surgery and the use of adhesion prevention barriers [10]
References
- Louwe PA, Badiola Gomez L, Webster H, Perona-Wright G, Bain CC, Forbes SJ, et al.. Recruited macrophages that colonize the post-inflammatory peritoneal niche convert into functionally divergent resident cells. . 2021. PMID 33741914 · DOI · PMC7979918
- Margry B, Kersemakers SC, Hoek A, Arkesteijn GJ, Wieland WH, van Eden W, et al.. Activated peritoneal cavity B-1a cells possess regulatory B cell properties. . 2014. PMID 24551182 · DOI · PMC3923827
- Ranzinger J, Rustom A, Abel M, Leyh J, Kihm L, Witkowski M, et al.. Nanotube action between human mesothelial cells reveals novel aspects of inflammatory responses. . 2011. PMID 22216308 · DOI · PMC3246504
- Tam H, Xu Y, An J, Schöneberg T, Schulz A, Muppidi JR, et al.. Phosphatidylserine phospholipase A1 enables GPR34-dependent immune cell accumulation in the peritoneal cavity. . 2024. PMID 39412501 · DOI · PMC11488134
- Dedrick RL, Flessner MF. Pharmacokinetic problems in peritoneal drug administration: tissue penetration and surface exposure. J Natl Cancer Inst. 1997. PMID 9086004 · DOI
- Donnez J, Binda MM, Donnez O, Dolmans MM. Oxidative stress in the pelvic cavity and its role in the pathogenesis of endometriosis. Fertil Steril. 2016. PMID 27521769 · DOI
- MIMS CA. ASPECTS OF THE PATHOGENESIS OF VIRUS DISEASES. Bacteriol Rev. 1964. PMID 14127970 · DOI · PMC441209
- Coccolini F, Cotte E, Glehen O, Lotti M, Poiasina E, Catena F, et al.. Intraperitoneal chemotherapy in advanced gastric cancer. Meta-analysis of randomized trials. Eur J Surg Oncol. 2014. PMID 24290371 · DOI
- Flessner MF. The transport barrier in intraperitoneal therapy. Am J Physiol Renal Physiol. 2005. PMID 15692055 · DOI
- DeCherney AH, diZerega GS. Clinical problem of intraperitoneal postsurgical adhesion formation following general surgery and the use of adhesion prevention barriers. Surg Clin North Am. 1997. PMID 9194886 · 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.