Silva C L, Faccioli L H
Department of Parasitology, Microbiology and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo, Brazil.
Infect Immun. 1988 Dec;56(12):3067-71. doi: 10.1128/iai.56.12.3067-3071.1988.
The mechanism by which cord factor (CF), a toxic glycolipid from mycobacteria, induces cachexia was studied in BALB/c mice. Body weight was markedly reduced 48 h after CF administration; the animals became severely wasted and exhibited hypertriglyceridemia, hypoglycemia, and high levels of tumor necrosis factor (TNF) in plasma. After CF administration, a transferable factor which caused cachexia and hypertriglyceridemia in recipient mice was detected in the blood. Dexamethasone partially inhibited the cachexia-inducing action of CF. Conditioned medium from adherent peritoneal cell cultures incubated with CF produced the same wasting symptoms when inoculated intravenously into mice. These studies also demonstrated that adherent peritoneal cells produced a humoral factor in response to CF which was related to CF-induced cachexia. Antiserum to recombinant TNF-alpha prevented the cachectin action in passive-transfer experiments. Our findings indicate that cachectin (TNF) plays a role as a central mediator of the wasting induced by CF.
研究了来自分枝杆菌的有毒糖脂——索状因子（CF）诱导恶病质的机制，实验对象为BALB/c小鼠。给予CF后48小时，体重显著下降；动物严重消瘦，出现高甘油三酯血症、低血糖，且血浆中肿瘤坏死因子（TNF）水平升高。给予CF后，在血液中检测到一种可转移因子，该因子可使受体小鼠出现恶病质和高甘油三酯血症。地塞米松部分抑制了CF诱导恶病质的作用。用CF孵育的贴壁腹膜细胞培养物的条件培养基静脉注射到小鼠体内时，产生了相同的消瘦症状。这些研究还表明，贴壁腹膜细胞对CF产生了一种体液因子，该因子与CF诱导的恶病质有关。在被动转移实验中，重组TNF-α抗血清可阻止恶病质素的作用。我们的研究结果表明，恶病质素（TNF）作为CF诱导消瘦的核心介质发挥作用。
