Cytokine-modulated inhibition of neutrophil apoptosis at local site augments exudative neutrophil functions and reflects inflammatory response after surgery

Background. The fate of exudative polymorphonuclear neutrophils (PMNs) at t he local site after surgery is not well understood. We evaluated the fate a nd functions of exudative PMNs at the local site in patients who were under going major surgery. We also investigated the relation between PMN apoptosi s and cytokine levels at the local site during the postoperative period. Methods. Exudative PMNs were isolated from II patients during the postopera tive period. Apoptosis, reactive oxygen intermediates (ROI) production, CD1 6, and tumor necrosis factor receptor expression of the PMNs were determine d by flow cytometry. Cytokine levels in the drainage fluid were measured. Results. Exudative PMN apoptosis was markedly inhibited on postoperative da y I and then increased in a time-dependent manner. IL-6 and granulocyte mac rophage colony-stimulating factor were significant factors to inhibit exuda tive PMN apoptosis; tumor necrosis factor-alpha and IL-10 were the factors to increase apoptosis. ROI production and CD16 expression of exudative PMNs were augmented when PMN apoptosis was inhibited in the early postoperative period. Conclusions. Exudative PMN apoptosis tons inhibited after surgery; PMN func tion was augmented after surgery. Cytokines at the local site may modulate exudative PMN apoptosis. Exudative PMN apoptosis reflected the inflammatory response after surgery. Understanding the mechanisms of PMN apoptosis and its pathophysiologic significance at local inflammatory sites in vivo may h elp in the design of more rational treatments.