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Effects of Prostaglandins on In Vivo Immune and Inflammatory Reactions

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Prostaglandins and Immunity

Part of the book series: Prostaglandins, Leukotrienes, and Cancer ((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.

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Authors
  1. Joseph C. Fantone
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  2. Steven L. Kunkel
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  3. Robert B. Zurier
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Editors and Affiliations

  1. Division of Gerontology, Department of Medicine, University of New Mexico School of Medicine, Albuquerque, NM, 87131, USA

    J. S. Goodwin

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© 1985 Martinus Nijhoff Publishing, Boston

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Fantone, J.C., Kunkel, S.L., Zurier, R.B. (1985). Effects of Prostaglandins on In Vivo Immune and Inflammatory Reactions. In: Goodwin, J.S. (eds) Prostaglandins and Immunity. Prostaglandins, Leukotrienes, and Cancer, vol 4. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2603-8_6

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  • DOI: https://doi.org/10.1007/978-1-4613-2603-8_6

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