ArticleInfection and immunity2014
Francisella tularensis LVS induction of prostaglandin biosynthesis by infected macrophages requires specific host phospholipases and lipid phosphatases.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Fatty acid metabolism and lipid channeling in macrophages: mechanisms of inflammation, resolution, and lipotoxicity.Frontiers in immunology · 2026Review
- Review
- Roles of Eicosanoids in Regulating Inflammation and Neutrophil Migration as an Innate Host Response to Bacterial Infections.Infection and immunity · 2021Article
- Modulation of Host Lipid Pathways by Pathogenic Intracellular Bacteria.Pathogens (Basel, Switzerland) · 2020Review
- Differential arterial and venous endothelial redox responses to oxidative stress.Microcirculation (New York, N.Y. : 1994) · 2018Article
- Host-based lipid inflammation drives pathogenesis inProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
- Immune Modulation as an Effective Adjunct Post-exposure Therapeutic for B. pseudomallei.PLoS neglected tropical diseases · 2016Article
- A Critical Role for Monocytes/Macrophages During Intestinal Inflammation-associated Lymphangiogenesis.Inflammatory bowel diseases · 2016Article
- Lipin-1 contributes to modified low-density lipoprotein-elicited macrophage pro-inflammatory responses.Atherosclerosis · 2015Article
- Acute rhabdomyolysis and inflammation.Journal of inherited metabolic disease · 2015Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Francisella tularensis induces the synthesis of prostaglandin E(2) (PGE(2)) by infected macrophages to alter host immune responses, thus providing a survival advantage to the bacterium. We previously demonstrated that PGE(2) synthesis by F. tularensis-infected macrophages requires cytosolic phospholipase A2 (cPLA(2)), cyclooxygenase 2 (COX-2), and microsomal prostaglandin E synthase 1 (mPGES1). During inducible PGE(2) synthesis, cPLA(2) hydrolyzes arachidonic acid (AA) from cellular phospholipids to be converted to PGE(2). However, in F. tularensis-infected macrophages we observed a temporal disconnect between Ser505-cPLA(2) phosphorylation (a marker of activation) and PGE(2) synthesis. These results suggested to us that cPLA(2) is not responsible for the liberation of AA to be converted into PGE(2) by F. tularensis-infected macrophages. Utilizing small-molecule inhibitors, we demonstrated that phospholipase D and diacylglycerol lipase were required for providing AA for PGE(2) biosynthesis. cPLA(2), on the other hand, was required for macrophage cytokine responses to F. tularensis. We also demonstrated for the first time that lipin-1 and PAP2a contribute to macrophage inflammation in response to F. tularensis. Our results identify both an alternative pathway for inducible PGE(2) synthesis and a role for lipid-modifying enzymes in the regulation of macrophage inflammatory function.
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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.