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Effects of Prostaglandins on In Vivo Immune and Inflammatory Reactions

Chapter
Part of the Prostaglandins, Leukotrienes, and Cancer book series (PLAC, volume 4)

Abstract

The initial observation of Kloeze in the 1960’s (1) that a metabolite of arachidonic acid, prostaglandin E (PGE), inhibited platelet aggregation led to the notion that cyclooxygenase products of arachidonic acid metabolism might have antiinflammatory activity. Subsequent studies demonstrating the ability of prostacyclin (PGI2) and PGE1 to inhibit platelet aggregation both in vitro and in vivo, and the production of relatively large quantities of PGI2 by endothelial cells served as a basis for defining one of the most important regulatory mechanisms involved in the initiation and progression of thrombus formation (reviewed in 2). Consequences of thrombosis (i.e. ischemia and infarction) are well known and serve as a basis for therapeutic strategies to modulate the onset and progression of myocardial and cerebral ischemia.

Keywords

Immune Complex Adjuvant Arthritis Arachidonic Acid Metabolism Arachidonic Acid Metabolite Formyl Peptide Receptor 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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© Martinus Nijhoff Publishing, Boston 1985

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