Allendoerfer R, Magee D M, Smith J G, Bonewald L, Graybill J R
Department of Medicine, University of Texas Health Science Center, San Antonio 78284.
J Infect Dis. 1993 May;167(5):1168-72. doi: 10.1093/infdis/167.5.1168.
Candidemia in humans is often associated with an endotoxic shock-like syndrome, comparable to gram-negative sepsis. Tumor necrosis factor-alpha (TNF alpha) has been implicated as a mediator in the endotoxic shock syndrome. The possible role of TNF alpha causing early deaths was explored in a murine model of acute infection with Candida albicans. In vitro data from three mouse strains (BALB/c, C3H/HeJ, and C3H/HeN) and in vivo data from BALB/c mice were obtained. Peritoneal macrophages from all three strains produced TNF alpha in vitro when stimulated with C. albicans. After intravenous infection with 10(8) cfu of C. albicans, mice died within 12 h. TNF concentrations in sera from these mice were significantly greater than in controls. Pretreatment of BALB/c mice with anti-murine TNF alpha did not alter mortality of C. albicans-infected mice, but pretreatment with murine TNF alpha reduced mortality. Therefore, in contrast to what was anticipated, TNF alpha may serve a protective role in murine candidiasis.
人类念珠菌血症常与一种类似内毒素休克的综合征相关，类似于革兰氏阴性菌败血症。肿瘤坏死因子-α（TNFα）被认为是内毒素休克综合征的介质。在白色念珠菌急性感染的小鼠模型中探讨了TNFα导致早期死亡的可能作用。获得了来自三种小鼠品系（BALB/c、C3H/HeJ和C3H/HeN）的体外数据以及来自BALB/c小鼠的体内数据。当用白色念珠菌刺激时，所有三种品系的腹膜巨噬细胞在体外均产生TNFα。静脉注射10⁸ cfu白色念珠菌后，小鼠在12小时内死亡。这些小鼠血清中的TNF浓度显著高于对照组。用抗小鼠TNFα对BALB/c小鼠进行预处理并未改变白色念珠菌感染小鼠的死亡率，但用小鼠TNFα进行预处理可降低死亡率。因此，与预期相反，TNFα在小鼠念珠菌病中可能起保护作用。
