ArticleThe Journal of clinical investigation1994
Lipopolysaccharide induces prostaglandin H synthase-2 protein and mRNA in human alveolar macrophages and blood monocytes.
Article in The Journal of clinical investigation, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 306 citations in OpenAlex.
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- Effect of regulated expression of human cyclooxygenase isoforms on eicosanoid and isoeicosanoid production in inflammation.The Journal of clinical investigation · 2000Trial
- Differential expression of eicosanoid pathways after whole blood stimulation in asthma patients.The World Allergy Organization journal · 2025Article
- Pulmonary surfactant and prostaglandin EPhysiological reports · 2024Article
- Polymer-free corticosteroid dimer implants for controlled and sustained drug delivery.Nature communications · 2021Article
- Dicer up-regulation by inhibition of specific proteolysis in differentiating monocytic cells.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Metabolic reprograming of LPS-stimulated human lung macrophages involves tryptophan metabolism and the aspartate-arginosuccinate shunt.PloS one · 2020Article
- TNFα Increases RANKL Expression via PGE₂-Induced Activation of NFATc1.International journal of molecular sciences · 2017Article
- Reinterpreting the best biomarker of oxidative stress: The 8-iso-prostaglandin F2α/prostaglandin F2α ratio shows complex origins of lipid peroxidation biomarkers in animal models.Free radical biology & medicine · 2016Article
- PAMAM dendrimers as nano carriers to investigate inflammatory responses induced by pulmonary exposure of PCB metabolites in Sprague-Dawley rats.Environmental science and pollution research international · 2016Article
- Protective Effect of Galectin-1 duringMediators of inflammation · 2016Article
- Reinterpreting the best biomarker of oxidative stress: The 8-iso-PGF(2α)/PGF(2α) ratio distinguishes chemical from enzymatic lipid peroxidation.Free radical biology & medicine · 2015Article
- 15-Hydroxyprostaglandin dehydrogenase generation of electrophilic lipid signaling mediators from hydroxy ω-3 fatty acids.The Journal of biological chemistry · 2015Article
- Nrf2 knockout attenuates the anti-inflammatory effects of phenethyl isothiocyanate and curcumin.Chemical research in toxicology · 2014Article
- Inhibition of nitric oxide production in LPS-stimulated RAW 264.7 cells by stem bark of Ulmus pumila L.Saudi journal of biological sciences · 2014Article
- Targeted proteomics of the eicosanoid biosynthetic pathway completes an integrated genomics-proteomics-metabolomics picture of cellular metabolism.Molecular & cellular proteomics : MCP · 2012Article
- Roflumilast inhibits the release of chemokines and TNF-α from human lung macrophages stimulated with lipopolysaccharide.British journal of pharmacology · 2012Article
- Prostaglandin E2 and the suppression of phagocyte innate immune responses in different organs.Mediators of inflammation · 2012Review
- Molecular Mechanisms Underlying Anti-Inflammatory Actions of 6-(Methylsulfinyl)hexyl Isothiocyanate Derived from Wasabi (Wasabia japonica).Advances in pharmacological sciences · 2012Article
- Cycloxygenase inhibition enhances the effects of surfactant therapy in endotoxin-induced rat model of ARDS.Inflammation · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We and others have previously demonstrated that human alveolar macrophages produce more PGE2 in response to lipopolysaccharide (LPS) than do blood monocytes. We hypothesized that this observation was due to a greater increase in prostaglandin H synthase-2 (PGHS-2) enzyme mass in the macrophage compared to the monocyte. To evaluate this hypothesis, alveolar macrophages and blood monocytes were obtained from healthy nonsmoking volunteers. The cells were cultured in the presence of 0 to 10 micrograms/ml LPS. LPS induced the synthesis of large amounts of a new 75-kD protein in human alveolar macrophages, and a lesser amount in monocytes. Synthesis of this protein required more than 6 h and peaked in 24 to 48 h; the protein reacted with an anti-PGHS-2 antibody prepared against mouse PGHS-2. Associated with synthesis of the protein was a marked increase in LPS-stimulated and arachidonic acid-stimulated synthesis of PGE2 by alveolar macrophages compared to monocytes. Cells not exposed to LPS contained only PGHS-1 and synthesized very little PGE2 during culture or in response to exogenous arachidonic acid. An LPS-induced mRNA, which hybridized to a human cDNA probe for PGHS-2 mRNA, was produced in parallel with production of this new protein and was produced in much greater amounts by alveolar macrophages compared to blood monocytes. This mRNA was not detectable in cells not exposed to LPS. In contrast, both types of cells contain mRNA, which hybridizes to a cDNA probe for PGHS-1. This mRNA did not increase in response to LPS. LPS also had no effect on PGHS-1 protein. These data demonstrate that PGE2 synthesis in human alveolar macrophages and blood monocytes correlates to the mass of PGHS-2 in the cell. We conclude that the greater ability of the macrophage to synthesize PGE2 in response to LPS is due to greater synthesis of PGHS-2 by the macrophage.
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Registered trials
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