Abstract
Eicosanoids are diverse mediators of inflammation that derive from a single cell membrane phospholipid- associated precursor, arachidonic acid. This precursor is metabolized to several groups of lipid mediators, including (but not limited to) prostaglandins, leukotrienes, and lipoxins, in a tightly regulated, coordinated, cell- and context-specific manner. Each mediator serves regulatory and homeostatic functions in the onset and resolution of inflammation, immune responses, and tissue repair. The cloning of biosynthetic enzymes and G protein-coupled receptors for each of these mediators, the development of transgenic mice deficient in these molecules, and the availability of selective antagonists have permitted studies that have rapidly expanded our understanding of the scope of biologic functions for these mediators, with potential ramifications for the pathogenesis and treatment of human asthma. This review summarizes these findings and reviews the data from both mouse and human studies pertinent to the pathobiologic role of each mediator.
Keywords: Eicosanoids, leukotrienes, prostaglandins, lipoxins
Current Molecular Medicine
Title: Eicosanoids in Asthma, Allergic Inflammation, and Host Defense
Volume: 8 Issue: 5
Author(s): Joshua A. Boyce
Affiliation:
Keywords: Eicosanoids, leukotrienes, prostaglandins, lipoxins
Abstract: Eicosanoids are diverse mediators of inflammation that derive from a single cell membrane phospholipid- associated precursor, arachidonic acid. This precursor is metabolized to several groups of lipid mediators, including (but not limited to) prostaglandins, leukotrienes, and lipoxins, in a tightly regulated, coordinated, cell- and context-specific manner. Each mediator serves regulatory and homeostatic functions in the onset and resolution of inflammation, immune responses, and tissue repair. The cloning of biosynthetic enzymes and G protein-coupled receptors for each of these mediators, the development of transgenic mice deficient in these molecules, and the availability of selective antagonists have permitted studies that have rapidly expanded our understanding of the scope of biologic functions for these mediators, with potential ramifications for the pathogenesis and treatment of human asthma. This review summarizes these findings and reviews the data from both mouse and human studies pertinent to the pathobiologic role of each mediator.
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Cite this article as:
Boyce A. Joshua, Eicosanoids in Asthma, Allergic Inflammation, and Host Defense, Current Molecular Medicine 2008; 8 (5) . https://dx.doi.org/10.2174/156652408785160989
DOI https://dx.doi.org/10.2174/156652408785160989 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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