Cytokines and PGE2 modulate the phagocytic function of the beta-glucan receptor in macrophages.
Under serum-free conditions the beta-glucan receptor of mouse macrophages mediates phagocytosis of beta-1,3-D-glucan-coated microbeads (diameter 2 microns). IFN-gamma increases the phagocytic function of the beta-glucan 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 phagocytic function of the beta-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-1 to macrophages. The effect disappears 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 the lowest phagocytic activity 9 h after addition of PGE2 to the cells.
Department of Experimental Pathology and Anatomy, Institute of Medical Biology, University of Tromsø, Norway.
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Konopski
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Seljelid
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Eskeland
D000818:Animals; D002478:Cells, Cultured; D016207:Cytokines / Q000494:pharmacology*; D015232:Dinoprostone / Q000494:pharmacology*; D004306:Dose-Response Relationship, Immunologic; D005260:Female; D005936:Glucans / Q000378:metabolism; D007371:Interferon-gamma / Q000494:pharmacology; D007375:Interleukin-1 / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects / Q000276:immunology*; D051379:Mice; D008863:Microspheres; D010587:Phagocytosis / Q000187:drug effects / Q000276:immunology*; D011956:Receptors, Cell Surface / Q000187:drug effects* / Q000276:immunology; D011951:Receptors, Complement / Q000187:drug effects / Q000276:immunology; D011971:Receptors, Immunologic; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D016207:Cytokines; D005936:Glucans; D007375:Interleukin-1; D011956:Receptors, Cell Surface; D011951:Receptors, Complement; D011971:Receptors, Immunologic; D014409:Tumor Necrosis Factor-alpha; C045268:beta-glucan receptor; D007371:Interferon-gamma; D015232:Dinoprostone