ArticleThe Journal of allergy and clinical immunology2014
Prostaglandin E₂ suppresses allergic sensitization and lung inflammation by targeting the E prostanoid 2 receptor on T cells.
Article in The Journal of allergy and clinical immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 67 citations in OpenAlex.
- Dietary and Plasma Polyunsaturated Fatty Acids Are Inversely Associated with Asthma and Atopy in Early Childhood.The journal of allergy and clinical immunology. In practice · 2019Trial
- Neither vaginal nor buccal administration of 800 μg misoprostol alters mucosal and systemic immune activation or the cervicovaginal microbiome: a pilot study.The European journal of contraception & reproductive health care : the official journal of the European Society of Contraception · 2016Trial
- A Functional Variant ofJournal of asthma and allergy · 2026Article
- Microbial sensing through the non-canonical inflammasome modulates airway type 2 immunity.Frontiers in immunology · 2026Article
- Membrane lipid composition of bronchial epithelial cells influences antiviral responses during rhinovirus infection.Tissue barriers · 2024Article
- Activation of the PGEFrontiers in immunology · 2024Article
- Endogenous inhibitory mechanisms in asthma.The journal of allergy and clinical immunology. Global · 2023Review
- IL-13-associated epithelial remodeling correlates with clinical severity in nasal polyposis.The Journal of allergy and clinical immunology · 2023Article
- Metabolic regulation by prostaglandin EAllergy · 2023Article
- The aryl hydrocarbon receptor regulates lipid mediator production in alveolar macrophages.Frontiers in immunology · 2023Article
- The Fusion Protein rFlaA:Betv1 Modulates DC Responses by a p38-MAPK and COX2-Dependent Secretion of PGECells · 2021Article
- Prostaglandin regulation of type 2 inflammation: From basic biology to therapeutic interventions.European journal of immunology · 2021Review
- Regulation, Activation and Function of Caspase-11 during Health and Disease.International journal of molecular sciences · 2021Review
- International Union of Basic and Clinical Pharmacology. CIX. Differences and Similarities between Human and Rodent Prostaglandin EPharmacological reviews · 2020Article
- Exophilin-5 regulates allergic airway inflammation by controlling IL-33-mediated Th2 responses.The Journal of clinical investigation · 2020Article
- The Biology of Prostaglandins and Their Role as a Target for Allergic Airway Disease Therapy.International journal of molecular sciences · 2020Review
- Resident alveolar macrophage-derived vesicular SOCS3 dampens allergic airway inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Caspase-11 promotes allergic airway inflammation.Nature communications · 2020Article
- PPARγ as an E3 Ubiquitin-Ligase Impedes Phosphate-Stat6 Stability and Promotes Prostaglandins EFrontiers in immunology · 2020Article
- Could Arachidonic Acid-Derived Pro-Resolving Mediators Be a New Therapeutic Strategy for Asthma Therapy?Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundEndogenous prostanoids have been suggested to modulate sensitization during experimental allergic asthma, but the specific role of prostaglandin (PG) E₂ or of specific E prostanoid (EP) receptors is not known.
objectiveHere we tested the role of EP2 signaling in allergic asthma.
methodsWild-type (WT) and EP2(-/-) mice were subjected to ovalbumin sensitization and acute airway challenge. The PGE2 analog misoprostol was administered during sensitization in both genotypes. In vitro culture of splenocytes and flow-sorted dendritic cells and T cells defined the mechanism by which EP2 exerted its protective effect. Adoptive transfer of WT and EP2(-/-) CD4 T cells was used to validate the importance of EP2 expression on T cells.
resultsCompared with WT mice, EP2(-/-) mice had exaggerated airway inflammation in this model. Splenocytes and lung lymph node cells from sensitized EP2(-/-) mice produced more IL-13 than did WT cells, suggesting increased sensitization. In WT but not EP2(-/-) mice, subcutaneous administration of misoprostol during sensitization inhibited allergic inflammation. PGE₂ decreased cytokine production and inhibited signal transducer and activator of transcription 6 phosphorylation by CD3/CD28-stimulated CD4(+) T cells. Coculture of flow cytometry-sorted splenic CD4(+) T cells and CD11c(+) dendritic cells from WT or EP2(-/-) mice suggested that the increased IL-13 production in EP2(-/-) mice was due to the lack of EP2 specifically on T cells. Adoptive transfer of CD4(+) EP2(-/-) T cells caused greater cytokine production in the lungs of WT mice than did transfer of WT CD4(+) T cells.
conclusionWe conclude that the PGE2-EP2 axis is an important endogenous brake on allergic airway inflammation and primarily targets T cells and that its agonism represents a potential novel therapeutic approach to asthma.
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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.