Cerami A, Ikeda Y, Le Trang N, Hotez P J, Beutler B
Immunol Lett. 1985;11(3-4):173-7. doi: 10.1016/0165-2478(85)90165-8.
Endotoxin-induced cells of the reticuloendothelial system were shown to produce mediator(s) that evoke a state of cachexia in recipient animals. The factor(s) responsible were assayed in endotoxin-resistant (C3H/HeJ) mice, which were injected with dialyzed conditioned medium obtained from lipopolysaccharide-induced peritoneal macrophages. The mice exhibited weight loss and anorexia, and they died if sufficient quantities of medium were administered. The syndrome was reversible if injections were discontinued. Endotoxin alone did not produce this effect, and no gross pathologic lesions were discernable in the treated animals. In this model system, cachexia appears to result from the action of soluble macromolecules produced by activated macrophages in vitro. Cachectin (murine tumor necrosis factor) is thought to play a central role in this phenomenon.
内毒素诱导的网状内皮系统细胞被证明能产生介质，这些介质会在受体动物中引发恶病质状态。在对内毒素有抗性的（C3H/HeJ）小鼠中检测了相关因子，这些小鼠被注射了从脂多糖诱导的腹腔巨噬细胞获得的透析条件培养基。小鼠出现体重减轻和厌食，如果给予足够量的培养基，它们会死亡。如果停止注射，该综合征是可逆的。单独的内毒素不会产生这种效应，并且在接受治疗的动物中没有明显的大体病理病变。在这个模型系统中，恶病质似乎是由体外活化巨噬细胞产生的可溶性大分子的作用导致的。恶病质素（小鼠肿瘤坏死因子）被认为在这一现象中起核心作用。
