Tumor necrosis factor-dependent adhesions as a major protective mechanism early in septic peritonitis in mice
Tumor necrosis factor-dependent adhesions as a major protective mechanism early in septic peritonitis in mice
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DOI：
10.1128/iai.69.6.3550-3555.2001
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发表时间：
2001-06-01
影响因子：
3.1
通讯作者：
Männel, DN
中科院分区：
文献类型：
--
作者：
Echtenacher, B;Weigl, K;Männel, DN
手术患者中腹膜粘连的发生与肿瘤坏死因子（TNF）水平正相关。在脓毒性腹膜炎-盲肠结扎和穿孔-TNF中和的模型中，防止了腹膜粘连的形成并增加了死亡率，这很可能是因为防止了脓毒性病灶的定位。为了区分非凝血依赖性保护性TNF效应和潜在的保护性促凝血TNF效应，用肝素、水蛭素或尿激酶抑制CLP后腹膜粘连的形成。每种治疗均不同程度地增加死亡率，并增加腹腔灌洗液、肾脏和肝脏中的细菌数量。在这些实验条件下，抗生素预防了死亡。在凝血功能受损的小鼠中，通过额外的TNF中和进一步增强了致死性。这些发现表明，脓毒性腹膜炎早期的腹膜粘连是先天免疫的重要机制，可防止细菌扩散增加并降低死亡率。
occurrence of peritoneal adhesions in surgical patients is positively correlated with tumor necrosis factor (TNF) levels, In a model of septic peritonitis-cecal ligation and puncture-TNF neutralization prevented formation of peritoneal adhesions and increased mortality, most likely because localization of the septic focus was prevented. To discriminate between the coagulation-independent protective TNF effect and a potential protective procoagulant TNF effect, formation of peritoneal adhesions after CLP was inhibited with heparin, hirudin, or urokinase, Each treatment increased mortality and increased the number of bacteria in the peritoneal lavage fluid, kidney, and liver to various degrees. Under these experimental conditions, antibiotics prevented death. In coagulation-compromised mice, lethality was further enhanced by additional TNF neutralization These findings demonstrate that peritoneal adhesions early in septic peritonitis are an important mechanism of innate immunity that prevents increased spread of bacteria and reduces mortality.