We demonstrated in the experimental sepsis model of cecal ligation and puncture (CLP) that TNF is essential for survival. The TNF required for protection acts via the p55TNF receptor as shown in experiments using TNF receptor-deficient mice. Pretreatment with IL-12 or injection of IFN#gamma# at the time of CLP rendered mice extremely sensitive for the lethal outcome of CLP. Experiments with mast cell-deficient mice have shown that mast cells are an ideal TNF source since they are capable of quickly providing stored TNF at the site of infection. The protective mechanism of TNF includes recruitment of granulocytes into the peritoneal cavity and their activation as well as generation of fibrin depositions for localization of the septic focus. These mechanisms of innate immunity are extremely important reactions of the organism for survival of septic peritonitis. (orig.)SIGLEAvailable from TIB Hannover: DtF QN1(67,30) / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekBundesministerium fuer Bildung, Wissenschaft, Forschung und Technologie, Bonn (Germany)DEGerman
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