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J Appl Physiol 79: 1271-1277, 1995;
8750-7587/95 $5.00
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Journal of Applied Physiology, Vol 79, Issue 4 1271-1277, Copyright © 1995 by American Physiological Society

ARTICLES

Modulation by dexamethasone of phospholipase A2 activities in endotoxemic guinea pigs

C. M. De Castro, M. F. Bureau, M. A. Nahori, C. H. Dumarey, B. B. Vargaftig and M. Bachelet
Unite de Pharmacologie Cellulaire, Unite Associee Institut Pasteur-Institut National de la Sante et de la Recherche Medicale 285, Paris, France.

One hour after lipopolysaccharide (LPS) administration (intravenous) in guinea pigs, alveolar macrophages are primed for an ex vivo increased secretion of arachidonic acid metabolites from the cyclooxygenase and the lipoxygenase pathways, with challenge by a second stimulus. At the same time, maximal levels of tumor necrosis factor-alpha (TNF-alpha) are observed in the circulation and in the bronchoalveolar lavage fluid. An extracellular form of phospholipase A2, corresponding probably to the low-molecular-mass type II enzyme, known to accumulate in inflammatory exudates, appears later in the serum of guinea pigs, to reach maximal levels 6 h after the LPS. Unlike the intracellular enzyme, extracellular phospholipase A2 is not increased by LPS in alveolar macrophages or in bronchoalveolar lavage fluids. After 24 h, at the time when neither TNF-alpha nor extracellular phospholipase A2 is present and priming of macrophages is over, maximal neutrophil infiltration is observed in the alveolar space of LPS-treated guinea pigs. Dexamethasone administered repeatedly during 3 days (subcutaneous) before the LPS challenge prevented both early events such as the macrophage priming and the TNF-alpha appearance and later events such as extracellular phospholipase A2 release and neutrophil recruitment.


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