The respiratory burst of murine alveolar macrophages (AM) was compared with that of peritoneal macrophages (PM). Superoxide anion (O
2-) 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 O
2-, whereas both macrophages released a large amount of O
2- 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 actibity to Candida parapsilosis. O
2- release of BCG-AM stimulated with zymosan was similer to that of BCG-PM. In both BCG-AM and BCG-PM, maximal O
2- response was obtained by stimulation with a lower concentration of zymosan than the concentration which required for resident macrophages to release maximal amount of O
2-. There was however, a remarkable difference between the ability of BCG-AM and BCG-PM to release O
2- when stimulated with PMA. Markedly enhanced O
2- release of BCG-PM was observed. In contrast, O
2- 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 O
2- release. Isoquinolinylsulfonyl piperadine (H-7), an inhibitor of protein kinase C, inhibited O
2- release of PMA-stimulated BCG-AM and BCG-PM in a dose-dependent manner and the extent of inhibition was greater in O
2- release of PM than that of AM. Superoxide anion release in response to zymosan was slightly inhibited by H-7. Dioctanoyl glycerol (DOG), a synthetic diacylglycerol, elicited a larger amount of O
2- release from BCG-PM than that of resident PM, whereas O
2- release of BCG-AM was no more than that of resident AM. These findings indicate that reactive oxygen intermediates (ROI) generation of AM differs significantly depending on the stimulant employed and O
2- response to PMA does not always correlate with the activation state of AM. Furthermore, these results suggest that more than two signal transduction pathways for the O
2--forming enzyme system may be present, and the activity of transduction pathway through protein kinase C might be low in murine AM. Since surfactant is an important environmental factor within the alveolar space, effect on O
2- release of AM was examined. Surfacten was purified from bovine alveolar lining material. When BCG-AM were incubated with various concentrations of surfacten, O
2- release of AM stimulated with PMA or zymosan was suppressed depending on the concentration of surfacten. Such inhibitory effect was greater in macrophages stimulated with PMA than with zymosan. Murine AM did not release a large amount of ROI to all stimuli, and even when activated, their responses were not enhanced uniformly. Taken together, such characteristics might release to a kind of host defense that protects lung tissue from possible delecterious effects of ROI.
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