ArticleJournal of immunology (Baltimore, Md. : 1950)2009
E-prostanoid 3 receptor deletion improves pulmonary host defense and protects mice from death in severe Streptococcus pneumoniae infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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.
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Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
- Persistent prostaglandin E2 upregulation and hormonal multi-resistance: A hypothesis for long COVID.Biochemistry and biophysics reports · 2026Article
- MicroRNA-155 Modulates Macrophages' Response to Non-Tuberculous Mycobacteria through COX-2/PGE2 Signaling.Pathogens (Basel, Switzerland) · 2021Article
- Decidual stromal cell-derived PGEAmerican journal of reproductive immunology (New York, N.Y. : 1989) · 2018Article
- The underestimated danger of E-cigarettes - also in the absence of nicotine.Respiratory research · 2018Article
- Ablation of the leptin receptor in myeloid cells impairs pulmonary clearance of Streptococcus pneumoniae and alveolar macrophage bactericidal function.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Identification of key genes in human airway epithelial cells in response to respiratory pathogens using microarray analysis.BMC microbiology · 2018Article
- Prostaglandin EPharmacology & therapeutics · 2018Review
- Inflammatory Resolution Triggers a Prolonged Phase of Immune Suppression through COX-1/mPGES-1-Derived Prostaglandin ECell reports · 2017Article
- Human lung fibroblasts produce proresolving peroxisome proliferator-activated receptor-γ ligands in a cyclooxygenase-2-dependent manner.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Article
- Increased lethality and defective pulmonary clearance of Streptococcus pneumoniae in microsomal prostaglandin E synthase-1-knockout mice.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Protective Effect of Galectin-1 duringMediators of inflammation · 2016Article
- Inflammatory Cyclooxygenase Activity and PGECurrent immunology reviews · 2015Article
- Aspirin enhances opsonophagocytosis and is associated to a lower risk for Klebsiella pneumoniae invasive syndrome.BMC infectious diseases · 2014Article
- Prospective diagnostic analysis of copy number variants using SNP microarrays in individuals with autism spectrum disorders.European journal of human genetics : EJHG · 2014Article
- Intrauterine group A streptococcal infections are exacerbated by prostaglandin E2.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Leukotriene B4 enhances innate immune defense against the puerperal sepsis agent Streptococcus pyogenes.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- PGE(2) suppression of innate immunity during mucosal bacterial infection.Frontiers in cellular and infection microbiology · 2013Review
- Cholera toxin induces a shift from inactive to active cyclooxygenase 2 in alveolar macrophages activated by Mycobacterium bovis BCG.Infection and immunity · 2013Article
- The resolution of inflammation.Nature reviews. Immunology · 2013Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Prostaglandins (PGs) are potent lipid mediators that are produced during infections and whose synthesis and signaling networks present potential pharmacologic targets for immunomodulation. PGE(2) acts through the ligation of four distinct G protein-coupled receptors, E-prostanoid (EP) 1-4. Previous in vitro and in vivo studies demonstrated that the activation of the G(alphas)-coupled EP2 and EP4 receptors suppresses inflammatory responses to microbial pathogens through cAMP-dependent signaling cascades. Although it is speculated that PGE(2) signaling via the G(alphai)-coupled EP3 receptor might counteract EP2/EP4 immunosuppression in the context of bacterial infection (or severe inflammation), this has not previously been tested in vivo. To address this, we infected wild-type (EP3(+/+)) and EP3(-/-) mice with the important respiratory pathogen Streptococcus pneumoniae or injected mice i.p. with LPS. Unexpectedly, we observed that EP3(-/-) mice were protected from mortality after infection or LPS. The enhanced survival observed in the infected EP3(-/-) mice correlated with enhanced pulmonary clearance of bacteria; reduced accumulation of lung neutrophils; lower numbers of circulating blood leukocytes; and an impaired febrile response to infection. In vitro studies revealed improved alveolar macrophage phagocytic and bactericidal capacities in EP3(-/-) cells that were associated with an increased capacity to generate NO in response to immune stimulation. Our studies underscore the complex nature of PGE(2) immunomodulation in the context of host-microbial interactions in the lung. Pharmacological targeting of the PGE(2)-EP3 axis represents a novel area warranting greater investigative interest in the prevention and/or treatment of infectious diseases.
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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.