ArticleJournal of immunology (Baltimore, Md. : 1950)2012
CRTH2 is a critical regulator of neutrophil migration and resistance to polymicrobial sepsis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 48 citations in OpenAlex.
- Epigenetic regulation of neutrophil dysfunction in sepsis: mechanisms, biomarkers, and translational challenges.Journal of translational medicine · 2026Review
- Molecular mechanisms and functions of protein acetylation in sepsis and sepsis-associated organ dysfunction.Cellular & molecular biology letters · 2025Review
- Prostacyclin synthase deficiency exacerbates systemic inflammatory responses in lipopolysaccharide-induced septic shock in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- mSignal transduction and targeted therapy · 2022Article
- Integrated analysis of DNA methylome and transcriptome reveals the differences in biological characteristics of porcine mesenchymal stem cells.BMC genomic data · 2021Article
- Crth2 receptor signaling down-regulates lipopolysaccharide-induced NF-κB activation in murine macrophagesFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- A CRTH2 antagonist, CT-133, suppresses NF-κB signalling to relieve lipopolysaccharide-induced acute lung injury.European journal of pharmacology · 2019Article
- Prostaglandin-cytokine crosstalk in chronic inflammation.British journal of pharmacology · 2019Review
- Sphingosine 1-phosphate receptor modulator ONO-4641 stimulates CD11bMucosal immunology · 2018Article
- Clarithromycin expands CD11b+Gr-1+ cells via the STAT3/Bv8 axis to ameliorate lethal endotoxic shock and post-influenza bacterial pneumonia.PLoS pathogens · 2018Article
- n-butanol extract from Folium isatidis inhibits the lipopolysaccharide-induced downregulation of CXCR1 and CXCR2 on human neutrophils.Molecular medicine reports · 2018Article
- Wip1 Deficiency Promotes Neutrophil Recruitment to the Infection Site and Improves Sepsis Outcome.Frontiers in immunology · 2017Article
- PKA regulatory IIα subunit is essential for PGD2-mediated resolution of inflammation.The Journal of experimental medicine · 2016Article
- Annexin A2 Modulates ROS and Impacts Inflammatory Response via IL-17 Signaling in Polymicrobial Sepsis Mice.PLoS pathogens · 2016Article
- Niacin Alternatives for Dyslipidemia: Fool's Gold or Gold Mine? Part I: Alternative Niacin Regimens.Current atherosclerosis reports · 2016Review
- Activation of the prostaglandin D2 metabolic pathway in Crohn's disease: involvement of the enteric nervous system.BMC gastroenterology · 2015Article
- TAT-SNAP-23 treatment inhibits the priming of neutrophil functions contributing to shock and/or sepsis-induced extra-pulmonary acute lung injury.Innate immunity · 2015Article
- Dyslipidaemia: cardiovascular prevention--end of the road for niacin?Nature reviews. Endocrinology · 2014Article
- CXCL1 contributes to host defense in polymicrobial sepsis via modulating T cell and neutrophil functions.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Neutrophil recruitment and function in health and inflammation.Nature reviews. Immunology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 5 institutions in 3 countries.
Funding
Abstract
Although arachidonic acid cascade has been shown to be involved in sepsis, little is known about the role of PGD(2) and its newly found receptor, chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2), on the septic response. Severe sepsis is associated with the failure of neutrophil migration. To investigate whether CRTH2 influences neutrophil recruitment and the lethality during sepsis, sepsis was induced by cecal ligation and puncture (CLP) surgery in mice. CRTH2 knockout (CRTH2(-/-)) mice were highly resistant to CLP-induced sepsis, which was associated with lower bacterial load and lower production of TNF-α, IL-6, and CCL3. IL-10, an anti-inflammatory cytokine, was higher in CRTH2(-/-) mice, blunting CLP-induced lethality in CRTH2(-/-) mice. Neutrophil accumulation in the peritoneum was more pronounced after CLP in CRTH2(-/-) mice, which was associated with higher CXCR2 levels in circulating neutrophils. Furthermore, sepsis caused a decrease in the level of acetylation of histone H3, an activation mark, at the CXCR2 promoter in wild-type neutrophils, suggesting that CXCR2 expression levels are epigenetically regulated. Finally, both pharmacological depletion of neutrophils and inhibition of CXCR2 abrogated the survival benefit in CRTH2(-/-) mice. These results demonstrate that genetic ablation of CRTH2 improved impaired neutrophil migration and survival during severe sepsis, which was mechanistically associated with epigenetic-mediated CXCR2 expression. Thus, CRTH2 is a potential therapeutic target for polymicrobial sepsis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.