Pulmonary defense mechanisms: modulation of Fc receptor activity in alveolar macrophages and other phagocytic cells by N-formyl peptides.

Abstract

Because the synthetic N-formyl peptides are similar in structure to products of bacterial metabolism, they may act similarly in providing signals of bacterial infection to phagocytic cells. With this in mind, we attempted to find out if N-formyl peptides increased Fc receptor activity in guinea pig alveolar macrophages, peritoneal macrophages, and neutrophils. N-formyl-methionyl-phenylalanine (FMP) and N-formyl-methionyl-L-leucyl-L-phenylalanine (FMLP) increased alveolar macrophage Fc receptor activity by 40 to 100%. The maximal increase in alveolar macrophage Fc receptor activity occurred after 2 h of in vitro incubation with 10(-6) M FMP. The increase in Fc receptor activity was blocked by cytochalasin B but not by colchicine, and did not appear to be related to morphologic alterations that were also induced by FMP. There was a similar increase in Fc receptor activity in peritoneal macrophages and neutrophils after in vitro exposure to FMP. For neutrophils, the increase was greatest after a 1-h incubation and with 10(5) M FMP. These results indicate that N-formyl peptides are stimulants of guinea pig phagocytic cell Fc receptor activity. Stimulation of Fc receptor activity may be one mechanism by which phagocytic cells combat bacterial infection in vivo.