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 (692 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 principal cyclooxygenase metabolite of arachidonic acid. It is released upon activation of mast cells and is also synthesized by alveolar macrophages. Among its many biological actions, the most important are its bronchoconstrictor, platelet-activating-factor-inhibitory, and cytotoxic effects.
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: D2, Prostaglandin; 11-Dehydroprostaglandin F2alpha; 11 Dehydroprostaglandin F2alpha; F2alpha, 11-Dehydroprostaglandin; 11-Dehydroprostaglandin F2 alpha; 11 Dehydroprostaglandin F2 alpha; alpha, 11-Dehydroprostaglandin F2; F2 alpha, 11-Dehydroprostaglandin.
Where it fits in the MeSH classification
- Broader topics
- Prostaglandins D
Research landscape
PubMed indexes 3,589 records tagged with the MeSH heading “Prostaglandin D2” (counts retrieved 2026-10-31). 219 of them (6.1%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,305 records.
Reviews account for 229 records (6.4%) and meta-analyses for 1. Randomized controlled trials number 50 (1.4%) 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 | 1,305 |
| 2000-2009 | 1,275 |
| 2010-2019 | 790 |
| 2020 onward | 219 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 229 | 6.4% |
| Meta-analyses | 1 | 0.0% |
| Randomized controlled trials | 50 | 1.4% |
Method: PubMed query "Prostaglandin D2"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
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 |
|---|---|---|---|---|
| Tumour-derived PGD2 and NKp30-B7H6 engagement drives an immunosuppressive ILC2-MDSC axis | 2017 | Research article Design not recorded in structured metadata | 208 | cc by PMID 28928446 · DOI · PMC5605498 |
| Neutrophils mediate Salmonella Typhimurium clearance through the GBP4 inflammasome-dependent production of prostaglandins | 2016 | Research article Design not recorded in structured metadata | 112 | cc by PMID 27363812 · DOI · PMC4932187 |
| Niacin ameliorates ulcerative colitis via prostaglandin D2-mediated D prostanoid receptor 1 activation | 2017 | Research article Design not recorded in structured metadata | 79 | cc by PMID 28341703 · DOI · PMC5412792 |
| Coactosin-Like Protein Reduces Prostaglandin D2 Production in Alveolar Macrophages and Alleviates Allergic Airway Inflammation | 2025 | Research article Design not recorded in structured metadata | 2 | cc by PMID 40569361 · DOI · PMC12442705 |
Tumour-derived PGD2 and NKp30-B7H6 engagement drives an immunosuppressive ILC2-MDSC axis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Group 2 innate lymphoid cells (ILC2s) are involved in human diseases, such as allergy, atopic dermatitis and nasal polyposis, but their function in human cancer remains unclear.
- Closing excerpt
- Here the authors show that, in acute promyelocytic leukaemia, tumour-activated ILC2s secrete IL-13 to induce myeloid-derived suppressor cells and support tumour growth.
- 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 (189 words)
Group 2 innate lymphoid cells (ILC2s) are involved in human diseases, such as allergy, atopic dermatitis and nasal polyposis, but their function in human cancer remains unclear. Here we show that, in acute promyelocytic leukaemia (APL), ILC2s are increased and hyper-activated through the interaction of CRTH2 and NKp30 with elevated tumour-derived PGD2 and B7H6, respectively. ILC2s, in turn, activate monocytic myeloid-derived suppressor cells (M-MDSCs) via IL-13 secretion. Upon treating APL with all-trans retinoic acid and achieving complete remission, the levels of PGD2, NKp30, ILC2s, IL-13 and M-MDSCs are restored. Similarly, disruption of this tumour immunosuppressive axis by specifically blocking PGD2, IL-13 and NKp30 partially restores ILC2 and M-MDSC levels and results in increased survival. Thus, using APL as a model, we uncover a tolerogenic pathway that may represent a relevant immunosuppressive, therapeutic targetable, mechanism operating in various human tumour types, as supported by our observations in prostate cancer.Group 2 innate lymphoid cells (ILC2s) modulate inflammatory and allergic responses, but their function in cancer immunity is still unclear. Here the authors show that, in acute promyelocytic leukaemia, tumour-activated ILC2s secrete IL-13 to induce myeloid-derived suppressor cells and support tumour growth.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28928446 · DOI · PMC5605498
Neutrophils mediate Salmonella Typhimurium clearance through the GBP4 inflammasome-dependent production of prostaglandins [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Inflammasomes are cytosolic molecular platforms that alert the immune system about the presence of infection.
- Closing excerpt
- Our results point to GBPs as key inflammasome adaptors required for prostaglandin biosynthesis and bacterial clearance by neutrophils and suggest that transient activation of the inflammasome may be used to treat bacterial infections.
- 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 (149 words)
Inflammasomes are cytosolic molecular platforms that alert the immune system about the presence of infection. Here we report that zebrafish guanylate-binding protein 4 (Gbp4), an IFNγ-inducible GTPase protein harbouring a C-terminal CARD domain, is required for the inflammasome-dependent clearance of Salmonella Typhimurium (ST) by neutrophils in vivo. Despite the presence of the CARD domain, Gbp4 requires the universal inflammasome adaptor Asc for mediating its antibacterial function. In addition, the GTPase activity of Gbp4 is indispensable for inflammasome activation and ST clearance. Mechanistically, neutrophils are recruited to the infection site through the inflammasome-independent production of the chemokine (CXC motif) ligand 8 and leukotriene B4, and then mediate bacterial clearance through the Gbp4 inflammasome-dependent biosynthesis of prostaglandin D2. Our results point to GBPs as key inflammasome adaptors required for prostaglandin biosynthesis and bacterial clearance by neutrophils and suggest that transient activation of the inflammasome may be used to treat bacterial infections.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27363812 · DOI · PMC4932187
Niacin ameliorates ulcerative colitis via prostaglandin D2-mediated D prostanoid receptor 1 activation [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Niacin, as an antidyslipidemic drug, elicits a strong flushing response by release of prostaglandin (PG) D2 However, whether niacin is beneficial for inflammatory bowel disease (IBD) remains unclear.
- Closing excerpt
- The potential efficacy of niacin in management of IBD warrants further investigation.
- 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 (166 words)
Niacin, as an antidyslipidemic drug, elicits a strong flushing response by release of prostaglandin (PG) D2 However, whether niacin is beneficial for inflammatory bowel disease (IBD) remains unclear. Here, we observed niacin administration-enhanced PGD2 production in colon tissues in dextran sulfate sodium (DSS)-challenged mice, and protected mice against DSS or 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in D prostanoid receptor 1 (DP1)-dependent manner. Specific ablation of DP1 receptor in vascular endothelial cells, colonic epithelium, and myeloid cells augmented DSS/TNBS-induced colitis in mice through increasing vascular permeability, promoting apoptosis of epithelial cells, and stimulating pro-inflammatory cytokine secretion of macrophages, respectively. Niacin treatment improved vascular permeability, reduced apoptotic epithelial cells, promoted epithelial cell update, and suppressed pro-inflammatory gene expression of macrophages. Moreover, treatment with niacin-containing retention enema effectively promoted UC clinical remission and mucosal healing in patients with moderately active disease. Therefore, niacin displayed multiple beneficial effects on DSS/TNBS-induced colitis in mice by activation of PGD2/DP1 axis. The potential efficacy of niacin in management of IBD warrants further investigation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28341703 · DOI · PMC5412792
Coactosin-Like Protein Reduces Prostaglandin D2 Production in Alveolar Macrophages and Alleviates Allergic Airway Inflammation [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Allergic asthma is a significant global health issue characterized by chronic airway inflammation.
- Closing excerpt
- These findings reveal that CLP modulates macrophage polarization and suppresses the PGD2-CRTH2 pathway to alleviate airway inflammation, highlighting CLP as a promising therapeutic target for asthma.
- 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)
Allergic asthma is a significant global health issue characterized by chronic airway inflammation. Current treatments only alleviate symptoms but fail to cure the disease due to its complex pathology. Lipid mediators from arachidonate metabolism are pivotal in immune regulation in asthma. Previously, coactosin-like protein (CLP) is identified as a regulator of leukotriene production in vitro. However, its role in asthma is unclear. In this study, it is found that CLP-deficient (Cotl1-/-) mice challenged with house dust mite (HDM) exhibits exacerbated airway inflammation, macrophage polarization, and type 2 immune responses. CLP deficiency increased prostaglandin D2 (PGD2) in bronchoalveolar lavage (BAL) and alveolar macrophages (AMs), activating the PGD2 receptor chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2) on immune cells. Notably, HDM exposure reduced pulmonary CLP levels in wild-type (WT) mice, and overexpression of CLP in Cotl1-/- macrophages decreased HDM-induced PGD2 in BAL and alleviated inflammation. Cotl1-/- AMs exacerbated HDM-induced airway inflammation compared to WT AMs, and this effect is dependent on CRTH2 signaling. These findings reveal that CLP modulates macrophage polarization and suppresses the PGD2-CRTH2 pathway to alleviate airway inflammation, highlighting CLP as a promising therapeutic target for asthma.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40569361 · DOI · PMC12442705
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 Prostaglandins as modulators of immunity [5]
- Research article 15d-PGJ2: the anti-inflammatory prostaglandin? [6]
- Research article Molecular mechanisms of sleep-wake regulation: roles of prostaglandins D2 and E2 [7]
- Research article Prostaglandins and adenosine in the regulation of sleep and wakefulness [8]
- Research article The role of adenosine in the regulation of sleep [9]
- Research article Biological activities and mechanisms of action of PGJ2 and related compounds: an update [10]
References
- Trabanelli S, Chevalier MF, Martinez-Usatorre A, Gomez-Cadena A, Salomé B, Lecciso M, et al.. Tumour-derived PGD2 and NKp30-B7H6 engagement drives an immunosuppressive ILC2-MDSC axis. . 2017. PMID 28928446 · DOI · PMC5605498
- Tyrkalska SD, Candel S, Angosto D, Gómez-Abellán V, Martín-Sánchez F, García-Moreno D, et al.. Neutrophils mediate Salmonella Typhimurium clearance through the GBP4 inflammasome-dependent production of prostaglandins. . 2016. PMID 27363812 · DOI · PMC4932187
- Li J, Kong D, Wang Q, Wu W, Tang Y, Bai T, et al.. Niacin ameliorates ulcerative colitis via prostaglandin D2-mediated D prostanoid receptor 1 activation. . 2017. PMID 28341703 · DOI · PMC5412792
- Pan LL, Ren Z, Li B, Liang W, Luo Y, Luo Y, et al.. Coactosin-Like Protein Reduces Prostaglandin D2 Production in Alveolar Macrophages and Alleviates Allergic Airway Inflammation. . 2025. PMID 40569361 · DOI · PMC12442705
- Harris SG, Padilla J, Koumas L, Ray D, Phipps RP. Prostaglandins as modulators of immunity. Trends Immunol. 2002. PMID 11864843 · DOI
- Scher JU, Pillinger MH. 15d-PGJ2: the anti-inflammatory prostaglandin?. Clin Immunol. 2005. PMID 15639643 · DOI
- Hayaishi O. Molecular mechanisms of sleep-wake regulation: roles of prostaglandins D2 and E2. FASEB J. 1991. PMID 1907936 · DOI
- Huang ZL, Urade Y, Hayaishi O. Prostaglandins and adenosine in the regulation of sleep and wakefulness. Curr Opin Pharmacol. 2007. PMID 17129762 · DOI
- Huang ZL, Urade Y, Hayaishi O. The role of adenosine in the regulation of sleep. Curr Top Med Chem. 2011. PMID 21401496 · DOI
- Fukushima M. Biological activities and mechanisms of action of PGJ2 and related compounds: an update. Prostaglandins Leukot Essent Fatty Acids. 1992. PMID 1438462 · 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.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
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.