CYTOKINES AND PGE2 MODULATE THE PHAGOCYTIC FUNCTION OF THE BETA-GLUCAN RECEPTOR IN MACROPHAGES

Under serum-free conditions the beta-glucan receptor of mouse macropha ges mediates phagocytosis of beta-1,3-D-glucan-coated microbeads (diam eter 2 mum). IFN-gamma increases the phagocytic function of the beta-g lucan receptor in a dose-dependent manner, giving the plateau level at 100 U/ml. Maximum activity appears 9 h after addition of IFN-gamma to the cells. The effect disappears within 24 h. The effect of IFN-gamma may be a result of augmented receptor synthesis since treatment with cycloheximide reduces the phagocytosis. IL-1 also increases the phagoc ytic function of the beta-glucan receptor giving a dose-dependent resp onse and with the plateau level reached at 10 U/ml. Maximum activity i s found 4 h after addition of IL-1 to macrophages. The effect disappea rs within 24 h. TNF does not alter the phagocytic function of the beta -glucan receptor, but TNF together with IL-1 prolongs the effect of IL -1. PGE2 reduces the phagocytic function of the beta-glucan receptor. Maximum reduction is achieved with 8 ng/ml. Time-course studies show t he lowest phagocytic activity 9 h after addition of PGE2 to the cells.