Cellular and molecular mechanisms of TNF protection in septic peritonitis.

Journal of inflammation Pub Date : 1995-01-01
B Echtenacher, L Hültner, D N Männel
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Abstract

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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TNF保护脓毒性腹膜炎的细胞和分子机制。
在小鼠盲肠结扎穿刺(CLP)模型中,内源性TNF对实验性脓毒性腹膜炎存活的要求已得到证实。在CLP之前诱导内源性TNF的产生或在CLP之前或之后给药TNF给予死亡保护。TNF与p55TNF受体的相互作用、纤维蛋白沉积的形成和粒细胞功能是CLP存活所必需的。肥大细胞似乎是该模型中提供保护所需TNF的重要细胞类型。
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