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Pretreatment of mice with low quantities of LPS induces endotoxin t olerance characterized by enhanced resistance to lethal doses of LPS and to a number of infectious challenges. M ice subjected to cecal ligation and puncture (CLP) survived the ensuing septic peritonitis significantly better when they had been pretreated with LPS. This LPS-induced protection was dependent on endogenous TNF production capacity since LPS pretreatment did not protect TNF-deficient mice from death after CLP. W hile mice deficient in the TNF receptor type 2 (p75TNFR) were as sensitive to CLP-induced mortality as control mice, LPS pretreatment could not reduce mortality in p75TNFR-deficient mice after CLP. Therefore, activation of the TNF receptor type 2 by endogenous TNF constitutes an important interaction for the development of LPS-induced resistance to bacterial infection.

Requirement of TNF and TNF receptor type 2 for LPS-induced protection from lethal septic peritonitis