Requirement of TNF and TNF receptor type 2 for LPS-induced protection from lethal septic peritonitis.
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.
Echtenacher
Bernd
B
Institute for Pathology and Tumor Immunology, University of Regensburg, Regensburg, Germany.
Männel
Daniela N
DN
D000818:Animals; D002432:Cecum / Q000293:injuries; D008070:Lipopolysaccharides / Q000633:toxicity*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010538:Peritonitis / Q000276:immunology* / Q000401:mortality; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000235:genetics* / Q000378:metabolism; D018805:Sepsis / Q000209:etiology / Q000276:immunology* / Q000401:mortality; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000235:genetics*
D008070:Lipopolysaccharides; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha