Protective action of thiols on neutrophil function

Abstract

A reduced chemotactic responsiveness of polymorphonuclear leukocytes (PMN) isolated from peripheral blood of smokers has previously been demonstrated and suggested to be an acute effect of smoking. The purpose of our studies were to determine: if the exposure of PMN to cigarette smoke in vitro inhibits chemotaxis; which fractions/components of smoke were the most potent inhibitors; the mechanism of chemotaxis inhibition. Whole smoke, the gas phase of smoke and the water-soluble fraction (WSF) of smoke condensate were all shown to be potent inhibitors of PMN chemotaxis. Upon fractionation of cigarette smoke condensate according to the polarity of the constituents, the polar fractions were the most potent inhibitors, while the nonpolar fractions were relatively weak inhibitors. Among the polar constituents tested the alpha, beta-unsaturated aldehyde, acrolein and crotonaldehyde were the most potent inhibitors of PMN chemotaxis. Cysteine completely protected PMN chemotaxis from the inhibitory effects of WSF, acrolein and crotonaldehyde, but provided only partial protection against the effects of whole cigarette smoke and the gas phase of smoke. Reduced glutathione completely protected against the effects of WSF and ony partially protected against the effects of the polar fractions of cigarette smoke. Impaired PMN chemotaxis as a result of smoke exposure may contribute to the increased susceptibility of heavy smokers to bronchopulmonary infections.