Arachidonic Acid Metabolites in Mediators of Inflammation
المؤلف:
Vinay Kumar, MBBS, MD, FRCPath; Abul K. Abbas, MBBS; Jon C. Aster, MD, PhD
المصدر:
Robbins & Cotran Pathologic Basis of Disease
الجزء والصفحة:
10th E ,P83-84
2025-11-08
77
The lipid mediators prostaglandins and leukotrienes are produced from arachidonic acid (AA) present in membrane phospholipids, and stimulate vascular and cellular reactions in acute inflammation. AA is a 20-carbon polyunsaturated fatty acid (5,8,11,14-eicosatetraenoic acid) that is derived from dietary sources or by conversion from the essential fatty acid linoleic acid. It does not occur free in the cell but is normally esterified in membrane phospholipids. Mechanical, chemical, and physical stimuli or other mediators (e.g., C5a) release AA from membrane phospholipids through the action of cellular phospholipases, mainly phospholipase A2. The biochemical signals involved in the activation of phospholipase A2 include an increase in cytoplasmic Ca2+ and activation of various kinases in response to external stimuli. AA-derived mediators, also called eicosanoids (because they are derived from 20-carbon fatty acids; Greek eicosa = 20), are synthesized by two major classes of enzymes: cyclooxygenases (which generate prostaglandins) and lipoxygenases (which produce leukotrienes and lipoxins) (Fig. 1). Eicosanoids bind to G protein-coupled receptors on many cell types and can mediate virtually every step of inflammation (Table 1).
Fig1. Production of arachidonic acid metabolites and their roles in inflammation. Note the enzymatic activities whose inhibition through pharmacologic intervention blocks major pathways (denoted with a red X). COX-1, COX-2, Cyclooxygenase 1 and 2; HETE, hydroxyeicosatetraenoic acid; HPETE, hydroperoxyeicosatetraenoic acid.
Table1. Principal Actions of Arachidonic Acid Metabolites in Inflammation
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