Neutrophils play an essential role in the host's defense against infection. Our previous studies have shown that blood and peritoneal neutrophils (PMN) have different basal activities and responses to infection. We also demonstrated that peritonitis produces divergent changes in the cellular function of PMN both in the blood and in the peritoneal fluid. Steroids are well documented to cause immunosuppression both clinically and, more variably, at the cellular level. Understanding the mechanism of steroid-induced immunosuppression in surgical infection may impart insight on the management of this condition. Using a model of surgical peritonitis, we studied the effects of immunosuppression on rabbit blood and peritoneal PMN. Blood and peritoneal PMNs were harvested after the development of fibrinopurulent peritonitis. Rabbits were divided into two groups: immunosuppressed and control. Immunosuppression was accomplished by intramuscular injection of dexamethasone (2 mg/kg) for 10 days preoperatively and 10 days postoperatively. Purified PMNs were studied for phagocytosis, adhesiveness, superoxide anion production and chemotaxis from both groups. Survival was computed from the number of days the rabbit survived after the operation up to a total of 10 at which time they were sacrificed. Immunosuppression with dexamethasone resulted in inhibition of peritoneal phagocytosis and peritoneal adhesiveness; there were no changes in blood adhesiveness nor blood phagocytosis. Also, there was no significant change in superoxide anion production nor in chemotaxis. Survival of the rabbits was significantly reduced when treated with dexamethasone. Based on these data, we conclude that (1) dexamethasone has different effects on infected blood and peritoneal PNN, (2) peritoneal PMN demonstrated decreased phagocytosis and adhesiveness with steroid immunosuppression, and (3) there was a decreased survival in rabbits that received dexamethasone with fibropurulent peritonitis.
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