Effect of hydrocortisone on macrophage response to lymphokine.
To define the suppressive effects of corticosteroids on mononuclear phagocyte antiprotozoal activity, normal resident peritoneal macrophages were exposed to hydrocortisone (HC) before, during, and after in vitro activation with cell-free supernatants (lymphokines). The presence of pharmacological concentrations of HC before or during lymphokine activation prevented normal macrophages from acquiring the capacity to either respond oxidatively to Toxoplasma gondii ingestion or to inhibit intracellular toxoplasma replication. HC had no effect, however, on the cells fully stimulated by lymphokine or on macrophages previously activated in vivo. These findings indicate that although HC does not impair the ability of activated macrophages to control intracellular protozoan infection, it does compromise the antimicrobial activity of the cell-mediated immune system by rendering normal macrophages unresponsive to lymphokine.
D000818:Animals; D006854:Hydrocortisone / Q000031:analogs & derivatives* / Q000494:pharmacology; D008222:Lymphokines / Q000494:pharmacology*; D008262:Macrophage Activation / Q000187:drug effects*; D008264:Macrophages / Q000187:drug effects* / Q000502:physiology; D008297:Male; D051379:Mice; D010101:Oxygen Consumption / Q000187:drug effects; D010587:Phagocytosis / Q000187:drug effects; D014122:Toxoplasma / Q000187:drug effects / Q000254:growth & development*
D008222:Lymphokines; C007133:hydrocortisone hemisuccinate; D006854:Hydrocortisone