Modulation of macrophage mannosyl-specific receptors by cultivation on immobilized zymosan. Effects on superoxide-anion release and phagocytosis.

Unopsonized zymosan effectively induces a respiratory burst (O-2 release, hexose monophosphate (HMP) shunt stimulation) in thioglycollate-elicited and BCG-activated macrophages (M phi). These M phi are known to express lectin-like receptors specific for mannose or fucose-terminated glycoconjugates (MFR). A role for the MFR in phagocytosis of zymosan was demonstrated by cultivating M phi on a glutaraldehyde-fixed layer of zymosan, a procedure which depleted M phi of MFR-mediated pinocytic activity, but not other surface antigens (F4/80, Mac-1) or receptors (FcR, C3R). After modulation of MFR, M phi lost the ability to phagocytose zymosan, but ingested antibody or complement-coated zymosan vigorously via alternative receptors. Challenge with free zymosan failed to enhance respiratory burst activity in M phi which had been cultivated on zymosan. Such M phi were also refractory to zymosan taken up by alternative receptors or other ingested particles (EIgG), but responded to a non-particulate challenge, PMA. These studies show that the MFR, like other receptors, can mediate phagocytosis and elicit a respiratory burst in suitably primed M phi, but indicate that phagocytosis via specific receptors (FcR, C3R) need not trigger a respiratory burst.