ArticleAmerican journal of respiratory cell and molecular biology2014
Prostaglandin E2 reduces Toll-like receptor 4 expression in alveolar macrophages by inhibition of translation.
Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03869268 (The Impact of Aspirin Dose Modification on the Innate Immune Response - Will Lower Dose Aspirin Therapy Reduce the Response to Endotoxin), which is not on this map. Cited by 16 papers.
What it found
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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.
The Impact of Aspirin Dose Modification on the Innate Immune Response - Will Lower Dose Aspirin Therapy Reduce the Response to Endotoxin
Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- The Role of PGE2 in Age-related Diseases.Current drug targets · 2025Review
- Molecular dynamics of inflammation resolution: therapeutic implications.Frontiers in cell and developmental biology · 2025Review
- Spinster homolog 2/S1P signaling ameliorates macrophage inflammatory response to bacterial infections by balancing PGECell communication and signaling : CCS · 2024Article
- Obesity Inhibits Alveolar Macrophage Responses to Pseudomonas aeruginosa Pneumonia via Upregulation of Prostaglandin E2 in Male, but Not Female, Mice.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Inhibition of COX-2 signaling favors E. coli during urinary tract infection.Journal of inflammation (London, England) · 2023Article
- Dynamics of inflammatory cytokine expression in bovine endometrial cells exposed to cow blood plasma small extracellular vesicles (sEV) may reflect high fertility.Scientific reports · 2023Article
- Age-induced prostaglandin ENature communications · 2022Article
- The Role of Glia in Addiction: Dopamine as a Modulator of Glial Responses in Addiction.Cellular and molecular neurobiology · 2022Review
- Concentrations of PGEPathogens (Basel, Switzerland) · 2022Article
- Myeloid-Specific Deficiency ofJournal of immunology (Baltimore, Md. : 1950) · 2021Article
- Prostaglandin EPharmacology & therapeutics · 2018Review
- Prostaglandin EFrontiers in physiology · 2017Review
- Beyond muscles: The untapped potential of creatine.International immunopharmacology · 2016Review
- Resolution of inflammation: a new therapeutic frontier.Nature reviews. Drug discovery · 2016Review
- Alveolar Epithelial Cell-Derived Prostaglandin E2 Serves as a Request Signal for Macrophage Secretion of Suppressor of Cytokine Signaling 3 during Innate Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Prostaglandin E₂ and polyenylphosphatidylcholine protect against intestinal fibrosis and regulate myofibroblast function.Digestive diseases and sciences · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Alveolar macrophages (AMs) represent the first line of innate immune defense in the lung. AMs use pattern recognition receptors (PRRs) to sense pathogens. The best studied PRR is Toll-like receptor (TLR)4, which detects LPS from gram-negative bacteria. The lipid mediator prostaglandin (PG)E2 dampens AM immune responses by inhibiting the signaling events downstream of PRRs. We examined the effect of PGE2 on TLR4 expression in rat AMs. Although PGE2 did not reduce the mRNA levels of TLR4, it decreased TLR4 protein levels. The translation inhibitor cycloheximide reduced TLR4 protein levels with similar kinetics as PGE2, and its effects were not additive with those of the prostanoid, suggesting that PGE2 inhibits TLR at the translational level. The action of PGE2 could be mimicked by the direct stimulator of cAMP formation, forskolin, and involved E prostanoid receptor 2 ligation and cAMP-dependent activation of unanchored type I protein kinase A. Cells pretreated with PGE2 for 24 hours exhibited decreased TNF-α mRNA and protein levels in response to LPS stimulation. Knockdown of TLR4 protein by small interfering RNA to the levels achieved by PGE2 treatment likewise decreased TNF-α mRNA and protein in response to LPS, establishing the functional significance of this PGE2 effect. We provide the first evidence of a lipid mediator acting through its cognate G protein-coupled receptor to affect PRR translation. Because PGE2 is produced in abundance at sites of infection, its inhibitory effects on AM TLR4 expression have important implications for host defense in the lung.
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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.