Thelestam M, Alouf J E, Geoffroy C, Möllby R
Infect Immun. 1981 Jun;32(3):1187-92. doi: 10.1128/iai.32.3.1187-1192.1981.
We investigated membrane damage to human diploid, embryonic lung fibroblasts caused by highly purified alveolysin by measuring leakage of cytoplasmic markers and uptake of various metabolites, and we observed a leakage pattern typical of SH-activated cytolysins. However, the mode of membrane interaction resembled the mode of membrane interaction of theta-toxin from Clostridium perfringens rather than that of streptolysin O in the following respects: the activity on fibroblast membranes was high compared with the activity on sheep erythrocytes; the toxin did not bind irreversibly to fibroblast cytoplasmic membranes; considerable membrane damage was caused at 0 degrees C; and inhibition of amino acid uptake occurred in the absence of significant structural membrane damage. These findings imply that data on membrane effects caused by streptolysin O cannot be related indiscriminately to other SH-activated cytolysins. With regard to the mode of membrane interaction, two apparently different groups of SH-activated cytolysins exist.
我们通过测量细胞质标记物的泄漏和各种代谢物的摄取，研究了高度纯化的肺泡溶血素对人二倍体胚胎肺成纤维细胞的膜损伤，并且我们观察到了一种典型的SH激活细胞溶素的泄漏模式。然而，在以下方面，膜相互作用模式类似于产气荚膜梭菌θ毒素的膜相互作用模式，而非链球菌溶血素O的膜相互作用模式：与对绵羊红细胞的活性相比，对成纤维细胞膜的活性较高；毒素不会不可逆地结合到成纤维细胞质膜上；在0℃时会造成相当大的膜损伤；并且在没有明显结构膜损伤的情况下会发生氨基酸摄取的抑制。这些发现表明，关于链球菌溶血素O引起的膜效应的数据不能不加区分地与其他SH激活细胞溶素相关联。关于膜相互作用模式，存在两组明显不同的SH激活细胞溶素。
