Cytokines and PGE2 Modulate the Phagocytic Function of the β‐Glucan Receptor in Macrophages

Under serum‐free conditions the β‐glucan receptor of mouse macrophages mediates phagocytosis of β‐l,3‐D‐glucan‐coated microbeads (diameter 2 μm). IFN‐γ increases the phagocytic function of the β‐glucan receptor in a dose‐dependent manner, giving the plateau level at 100 U/ml. Maximum activity appears 9 h after addition of IFN‐γ to the cells. The effect disappears within 24 h. The effect of IFN‐γ may be a result of augmented receptor synthesis since treatment with cycloheximide reduces the phagocytosis. IL‐1 also increases the phagocytic function of the β‐glucan receptor giving a dose‐dependent response and with the plateau level reached at 10 U/ml. Maximum activity is found 4 h after addition of IL‐I to macrophages. The effect disappears within 24 h. TNF does not alter the phagocytic function of the β‐glucan receptor, but TNF together with IL‐1 prolongs the effect of IL‐1. PGE2 reduces the phagocytic function of the β‐glucan receptor. Maximum reduction is achieved with 8 ng/ml. Time‐course studies show the lowest phagocytic activity 9 h after addition of PGE2 to the cells.