Inhibitory effect of glucocorticoid on complement activation induced by lipopolysaccharide.
Endotoxic lipopolysaccharide is verified to activate complement, which seems to be one of the major pathogenic processes of septic shock, and glucocorticoid antagonizes this endotoxic manifestation in a dose-related manner. In this study, we tried to elucidate how lipopolysaccharide activates complement in vitro, and how glucocorticoid affects the interaction between them. First, we elucidated in vitro that complement was consumed in proportion to the dose of lipopolysaccharide added. Next we made clear that glucocorticoids inhibit the complement activation by lipopolysaccharide in a dose-related manner in vitro, and the dose that inhibits endotoxic complement activation by 50% was almost the same for hydrocortisone, prednisolone, and dexamethasone. We conclude that lipopolysaccharide activates complement in a dose-related manner and that glucocorticoids inhibit this activation in a dose-related manner, and this may be the main antiendotoxic property of glucocorticoids.
D003167:Complement Activation / Q000187:drug effects*; D003165:Complement System Proteins; D003907:Dexamethasone / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology*; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology; D066298:In Vitro Techniques; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D011239:Prednisolone / Q000494:pharmacology
D005938:Glucocorticoids; D008070:Lipopolysaccharides; D003907:Dexamethasone; D003165:Complement System Proteins; D011239:Prednisolone; D006854:Hydrocortisone