Inhibition of yeast phagocytosis and cell spreading by glucocorticoids in cultures of resident murine peritoneal macrophages.
This study was initiated to determine whether the inhibition of phagocytosis and cell spreading in cortisol-treated cultures of resident murine peritoneal macrophages are glucocorticoid-directed responses. Phagocytosis of heat-killed Saccharomyces cerevisiae and cell spreading were measured in control and steroid-treated macrophage cultures over 6 days. When the cultures were exposed to testosterone, progesterone, or epicortisol, phagocytosis and cell spreading were similar to controls. In contrast, both macrophage functions were inhibited significantly in cultures treated with cortisol, methylprednisolone, dexamethasone, and triamcinolone acetonide. In addition, the rate of phagocytosis was retarded and phagocytic indices (i.e., yeast particle number/cell) were reduced in glucocorticoid-treated cultures. Dose-response studies with dexamethasone demonstrated that the ED50 for the inhibitory effect on phagocytosis was 20 nM. These results indicate that the inhibition of yeast phagocytosis and cell spreading in the steroid-treated cultures are specific glucocorticoid-directed responses.
D000818:Animals; D001202:Ascitic Fluid / Q000166:cytology; D002478:Cells, Cultured; D003907:Dexamethasone / Q000494:pharmacology; D005938:Glucocorticoids / Q000494:pharmacology*; D008264:Macrophages / Q000166:cytology / Q000187:drug effects* / Q000276:immunology; D051379:Mice; D010587:Phagocytosis / Q000187:drug effects*; D012441:Saccharomyces cerevisiae; D013256:Steroids / Q000494:pharmacology
D005938:Glucocorticoids; D013256:Steroids; D003907:Dexamethasone