Cellular changes in association with defense mechanisms in intra-abdominal sepsis.

Despite progress, intra-abdominal sepsis is associated with a high morbitity and mortality rate. Although, much effort has been made in basic research, there have not been any therapeutic applications as yet. The peritoneal defense system (innate and specific) represents the first local reaction to inflammation caused by bacterial invasion. It includes lymphatic absorption of bacteria, phagocytosis, entrenchment of inflammation and lymphocyte production (humoral and cellular immune). Also, the fibrin formation and degradation by intraperitoneal activation of coagulation and fibrinolysis plays an important role in this local response. The endotoxin from Gram-negative or exotoxins from Gram-positive bacteria cause the release of proinflammatory cytokines (TNF-alpha, IL-1betha, IL-6) by macrophages. They act as mediators resulting in the initiation of systemic inflammatory response syndrome (SIRS) at first and cellular damage with multiple organ dysfunction syndrome (MODS) ultimately. There are two different, but communicated, functional departments, i.e. peritoneal and systemic compromising the host inflammatory response to bacterial infection. Cytokine production occurs in both of them.