The clinical course of secondary peritonitis strongly depends on the s
ystemic inflammatory host response of patients. The controlled activat
ion of leukocytes (local, emigrated) in the abdomen with consecutive p
roduction of different cytokines is necessary for the killing of micro
organisms. But about 10-20 % of patients with peritonitis develop - de
spite aggressive surgical treatment and antibiotic therapy -, sepsis a
nd multiple organ failure. This might be related to an augmented syste
mic inflammatory response with an uncontrolled production of proinflam
matory cytokines. In experimental and some clinical studies of periton
itis pro but also antiinflammatory cytokines have been found in the bl
ood and in the peritoneal exudate. The concentration of cytokines in t
he peritoneal exudate were several times higher than in the blood. In
future therapy concepts of peritonitis the modulation of leukocyte act
ivation and cytokine production looks interesting and should be consid
ered in a local and systemic manner.