Comparison of wheat germ agglutinin- and phorbol myristate acetate-mediated triggering for macrophage H2O2 release: susceptibilities to various macrophage inhibitors.

Murine peritoneal macrophages (M phi S) elicited by a single injection of zymosan A showed a higher responsiveness to the wheat germ agglutinin (WGA)-mediated triggering for H2O2 release than M phi S activated by double injections of the agent. On the contrary, the response to phorbol myristate acetate(PMA)-mediated triggering was higher in the latter M phi S than in the case of the former M phi S. Furthermore, PMA-triggered M phi H2O2 release was found to be inhibited by sarcoma 180 tumor cell-derived proteinaceous factor in a much more marked fashion than the WGA-triggered H2O2 release. These results indicate some significant differences between the cellular mechanisms of the WGA- and PMA-triggering for M phi oxidative burst. On the other hand, microfilament-inhibitors (cytochalasins B and E) and serine protease-inhibitors (tosyl-L-lysine-chloromethyl ketone and tosylamido-2-phenylethyl-chloromethyl ketone), but not microtubule-disrupting agents (colchicine, vinblastine, and vincristine), suppressed both the WGA- and PMA-triggerings for M phi H2O2 release to a similar degree, thereby indicating that the WGA- and PMA-triggerings for M phi oxidative burst have a common process which is dependent on microfilament and serine protease functions. In relation to this, the WGA- and PMA-triggerings for M phi spreading were also depressed by microfilament- and serine protease-inhibitors but not by microtubule-inhibitors, indicating a participation of common membrane functions in the signal transduction in cases of M phi oxidative burst, and cell spreading induced by the WGA- as well as PMA-triggering.