Effects of endotoxins and cytokines on the secretion of platelet-activating factor-acetylhydrolase by human decidual macrophages.

Abstract

The aim was to clarify the role of platelet-activating factor in parturition, preterm labor, and premature rupture of membranes. Decidual macrophage populations were obtained by enzymic digestion, Ficoll-Paque centrifugation, or flow cytometric sorting. The effects of endotoxins and cytokines on platelet-activating factor-acetylhydrolase secretion by these cells were examined. Lipopolysaccharide inhibited the platelet-activating factor-acetylhydrolase secretion by decidual macrophages. The inhibition was partially reversed by interleukin-1 receptor antagonist or by neutralizing antibodies against interleukin-1 alpha, interleukin-1 beta, or tumor necrosis factor-alpha. Tumor necrosis factor-alpha, interleukin-1 alpha, and interleukin-1 beta also decreased the enzyme secretion. The inhibitory actions of tumor necrosis factor-alpha and interleukin-1 beta were specifically neutralized by the corresponding antibodies. The effect of interleukin-1 alpha or interleukin-1 beta on the secretion was abolished by interleukin-1 receptor antagonist. It is suggested that platelet-activating factor is involved in the pathogenesis of preterm labor or premature rupture of membranes caused by endotoxins and the subsequent activation of cytokine network.