{"title":"TNF保护脓毒性腹膜炎的细胞和分子机制。","authors":"B Echtenacher, L Hültner, D N Männel","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Requirement for endogenous TNF for survival of experimental septic peritonitis has been demonstrated in a mouse model of cecal ligation and puncture (CLP). Induction of endogenous TNF production before CLP or administration of TNF before or after CLP confered protection from death. Interaction of TNF with the p55TNF receptor, formation of fibrin deposits, and granulocyte function was necessary to survive CLP. The mast cell seems to be an important cell type to provide the TNF required for protection in this model.</p>","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"47 1-2","pages":"85-9"},"PeriodicalIF":0.0000,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Cellular and molecular mechanisms of TNF protection in septic peritonitis.\",\"authors\":\"B Echtenacher, L Hültner, D N Männel\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Requirement for endogenous TNF for survival of experimental septic peritonitis has been demonstrated in a mouse model of cecal ligation and puncture (CLP). Induction of endogenous TNF production before CLP or administration of TNF before or after CLP confered protection from death. Interaction of TNF with the p55TNF receptor, formation of fibrin deposits, and granulocyte function was necessary to survive CLP. The mast cell seems to be an important cell type to provide the TNF required for protection in this model.</p>\",\"PeriodicalId\":79405,\"journal\":{\"name\":\"Journal of inflammation\",\"volume\":\"47 1-2\",\"pages\":\"85-9\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1995-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of inflammation\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of inflammation","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Cellular and molecular mechanisms of TNF protection in septic peritonitis.
Requirement for endogenous TNF for survival of experimental septic peritonitis has been demonstrated in a mouse model of cecal ligation and puncture (CLP). Induction of endogenous TNF production before CLP or administration of TNF before or after CLP confered protection from death. Interaction of TNF with the p55TNF receptor, formation of fibrin deposits, and granulocyte function was necessary to survive CLP. The mast cell seems to be an important cell type to provide the TNF required for protection in this model.
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