Release of oxygen products from lung macrophages by N-formyl peptides.

Abstract

Incubation of guinea pig pulmonary macrophages with N-formylmethionylphenylalanine (FMP) resulted in 1) a rapid increase in O2 consumption and 2) an accumulation of superoxide anion and hydrogen peroxide in the extracellular medium. The accumulation of superoxide anion and hydrogen peroxide was completely prevented in the presence of superoxide dismutase and catalase, respectively. FMP-stimulated O2 consumption and superoxide anion and hydrogen peroxide accumulation were proportional to the macrophage concentration, showed similar dependence on FMP concentration, had nearly identical kinetics, and were partially abolished by antimycin A, an inhibitor of mitochondrial respiration. FMP also stimulated a three- to fourfold increase in hexose monophosphate shunt (HMS) activity. Catalase had no effect on the amount of glucose oxidized by the HMS, indicating that removal of hydrogen peroxide was without effect on the observed HMS activity. Since FMP is similar in structure to the oligopeptides of bacterial metabolism, its ability to stimulate the release of these microbiocidal products of oxygen metabolism may be important in vivo.