Effect of cyclic adenosine 3',5'-monophosphate antagonists on endotoxin-induced inhibition of human neutrophil chemotaxis

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Abstract
Escherichia coli endotoxin [etox] inhibited human neutrophil chemotaxis toward C5a [fragment a of complement component 5]. This effect of etox was antagonized by anti-inflammatory steroids. Dibutyryl cyclic[c]AMP, prostaglandin [PG] E1, isoproterenol and cholera toxin antagonize the suppression of chemotaxis by etox. Each compound inhibited the effect of etox in a dose-dependent fashion. To be effective, each compound except cholera toxin had to be present at the time of etox challenge. Propranolol blocked the protective effect of isoproterenol against etox but not the protective effect of dibutyryl cAMP or PGE1. Dibutyryl cGMP, AMP, phenylephrine, PGF2.alpha. and carbachol did not modify the suppression of chemotaxis by etox. Anti-inflammatory steroids and dibutyryl cAMP may stabilize phospholipids in certain cell membranes. This phospholipid-stabilizing action may partly contribute to the protective effect against etox-mediated suppression of neutrophil chemotaxis.