Oxygen radical generation of murine alveolar macrophages

Abstract

The respiratory burst of murine alveolar macrophages (AM) was compared with that of peritoneal macrophages (PM). Superoxide anion (O2-) released from resident AM was similar to that of resident PM. That is, resident AM or PM exposed to phorbol myristate acetate (PMA) released only a small amount of O2-, whereas both macrophages released a large amount of O2- when stimulated with zymosan particles. AM as well as PM obtained from mice injected with Mycobacterium bovis BCG 3 weeks previously (abbreviated to BCG-AM and BCG-PM, respectively) showed an enhanced killing activity to Candida parapsilosis. O2- release of BCG-AM stimulated with zymosan was similar to that of BCG-PM. In both BCG-AM and BCG-PM, maximal O2- response was obtained by stimulation with a lower concentration of zymosan than the concentration which required for resident macrophages to release maximal amount of O2-. There was however, a remarkable difference between the ability of BCG-AM and BCG-PM to release O2- when stimulated with PMA. Markedly enhanced O2- release of BCG-PM was observed. In contrast, O2- release of BCG-AM exposed to PMA was almost the same as that of resident AM. Hydrogen peroxide release of BCG-AM, when stimulated with PMA or zymosan, was compatible with O2- release. Isoquinolinylsulfonyl piperadine (H-7), an inhibitor of protein kinase C, inhibited O2- release of PMA-stimulated BCG-AM and BCG-PM in a dose-dependent manner and the extent of inhibition was greater in O2- release of PM than that of AM. Superoxide anion release in response to zymosan was slightly inhibited by H-7.(ABSTRACT TRUNCATED AT 250 WORDS)