Zusammenfassung
Pretreatment of mice with low quantities of LPS induces endotoxin tolerance characterized by enhanced resistance to lethal doses of LPS and to a number of infectious challenges. Mice 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 ...
Zusammenfassung
Pretreatment of mice with low quantities of LPS induces endotoxin tolerance characterized by enhanced resistance to lethal doses of LPS and to a number of infectious challenges. Mice 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. While 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.
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