Barrett T J, Potter M E, Strockbine N A
Division of Bacterial Diseases, Centers for Disease Control, Atlanta, Georgia 30333.
Microb Pathog. 1990 Aug;9(2):95-103. doi: 10.1016/0882-4010(90)90083-3.
Seven strains of inbred mice were compared for their susceptibility to the lethal effects of Shiga-like toxin II (SLT II). A/J mice, which are unable to produce the C5 component of complement, did not differ from C5 normal mice in susceptibility to SLT II. CBA/NJ mice (hemizygous for X-linked immunodeficiency) did not differ from the B-cell sufficient CBA/J strain. C3H/HeJ mice, defective in macrophage response to lipopolysaccharide (Lpsd), showed a consistently and significantly longer mean time to death than did the normally responsive C3H/HeN strain. C57BL/10ScN mice, which also carry the Lpsd allele, showed a similar but smaller difference in mean time to death compared with the C57BL/10SnJ strain. Production of tumor necrosis factor could be induced in vitro by SLT II treatment of C3H/HeN, but not C3H/HeJ macrophages. These results imply that antibody and complement production do not modulate SLT II lethality in mice, but that the macrophage may contribute to SLT II-induced injury.
对七种近交系小鼠进行了比较，以研究它们对志贺样毒素II（SLT II）致死作用的易感性。不能产生补体C5成分的A/J小鼠，在对SLT II的易感性方面与C5正常小鼠没有差异。CBA/NJ小鼠（X连锁免疫缺陷半合子）与B细胞充足的CBA/J品系没有差异。巨噬细胞对脂多糖（Lpsd）反应缺陷的C3H/HeJ小鼠，与正常反应的C3H/HeN品系相比，平均死亡时间持续且显著更长。同样携带Lpsd等位基因的C57BL/10ScN小鼠，与C57BL/10SnJ品系相比，平均死亡时间的差异相似但较小。用SLT II处理C3H/HeN巨噬细胞可在体外诱导肿瘤坏死因子的产生，但处理C3H/HeJ巨噬细胞则不能。这些结果表明，抗体和补体的产生不会调节小鼠对SLT II的致死性，但巨噬细胞可能参与了SLT II诱导的损伤。
