Modulation of lipid and protein mediators of inflammation by cytosolic phospholipase A2alpha during experimental sepsis

The Journal of Immunology : Official Journal of the American Association of Immunologists
Naonori UozumiTakao Shimizu

Abstract

Cytosolic phospholipase A(2)alpha (cPLA(2)alpha) is one of the key enzymes in lipid mediator generation. It preferentially hydrolyzes arachidonoyl-phospholipid in response to cellular stimuli, liberating arachidonic acid, the shared precursor of PGs and leukotrienes. Mice with disruption of the cPLA(2)alpha gene exhibit a more than 80% decrease in the generation of these lipid mediators, leading to dramatic phenotypes in various models of inflammatory and allergic disease. In this study, we use the cecal ligation and puncture model of sepsis along with multiplex quantitation systems to explore interactions between eicosanoids and protein mediators. cPLA(2)alpha-deficient mice exhibited significantly less weight loss accompanied by decreased generation of PGs, leukotriene B(4), IL-6, and CCL2. Despite these differences, genetic ablation of cPLA(2)alpha did not provide any survival advantage. Unexpectedly, abundant production of 12-hydroxy-eicosatetraenoic acid, another arachidonic acid-derived lipid mediator, was found to be unaffected by disruption of the cPLA(2)alpha gene. Eicosanoid production preceded the production of cytokines. Eicosanoid modulation of IL-6 and CCL2 expression was suggested by scattergram analyses. These r...Continue Reading

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Apr 4, 2015·Journal of Lipid Research·Christina C Leslie
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