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首页> 外文期刊>Infection and immunity >Synergistic Effects of Alpha-Toxin and Perfringolysin O in Clostridium perfringens-Mediated Gas Gangrene
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Synergistic Effects of Alpha-Toxin and Perfringolysin O in Clostridium perfringens-Mediated Gas Gangrene

机译：产气荚膜梭菌介导的气体坏疽中α-毒素和产球菌溶血素O的协同作用

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To examine the synergistic effects of alpha-toxin and perfringolysin O in clostridial myonecrosis, homologous recombination was used to construct an alpha-toxin deficient derivative of a perfringolysin O mutant of Clostridium perfringens. The subsequent strain was complemented with separate plasmids that carried the alpha-toxin structural gene (plc), the perfringolysin O gene (pfoA), or both toxin genes, and the resultant isogenic strains were examined in a mouse myonecrosis model. Synergistic effects were clearly observed in these experiments. Infection with the control strain, which did not produce either toxin, resulted in very minimal gross pathological changes, whereas the isogenic strain that was reconstituted for both toxins produced a pathology that was clearly more severe than when alpha-toxin alone was reconstituted. These changes were most apparent in the rapid spread of the disease, the gross pathology of the footpad and in the rate at which the mice had to be euthanatized for ethical reasons. Elimination of both alpha-toxin and perfringolysin O production removed most of the histopathological features typical of clostridial myonecrosis. These effects were restored when the mutant was complemented with the alpha-toxin structural gene, but reconstituting only perfringolysin O activity produced vastly different results, with regions of coagulative necrosis, apparently enhanced by vascular disruption, being observed. Reconstitution of both alpha-toxin and perfringolysin O activity produced histopathology most similar to that observed with the alpha-toxin reconstituted strain. The spreading of myonecrosis was very rapid in these tissues, and coagulative necrosis appeared to be restricted to the lumen of the blood vessels. The results of these virulence experiments clearly support the hypothesis that alpha-toxin and perfringolysin O have a synergistic effect in the pathology of gas gangrene.
机译：为了检测α-毒素和穿孔素溶血素O在梭菌性肌坏死中的协同作用，采用同源重组构建了产气荚膜梭菌的穿孔素溶血素O突变体的α-毒素缺陷型衍生物。随后的菌株补充了带有α-毒素结构基因（ plc），产气荚膜溶素O基因（ pfoA ）或两个毒素基因的单独质粒，在小鼠骨髓坏死模型中检查了同基因菌株。在这些实验中清楚地观察到了协同作用。不产生任何毒素的对照菌株的感染导致非常小的总体病理变化，而针对两种毒素重构的同基因菌株产生的病理学明显比仅重组α-毒素时更为严重。这些改变在疾病的迅速传播，脚垫的总体病理以及出于伦理原因必须对小鼠实施安乐死的速度中最为明显。消除α-毒素和产气荚膜溶血素O的产生消除了梭菌性肌坏死典型的大多数组织病理学特征。当突变体与α-毒素结构基因互补时，这些作用得以恢复，但是仅重组穿孔蛋白溶素O活性产生了截然不同的结果，观察到凝血坏死区域明显被血管破坏所增强。重组α-毒素和穿孔蛋白溶素O的活性产生的组织病理学与用α-毒素重组菌株观察到的最为相似。骨髓坏死在这些组织中的扩散非常迅速，而凝血坏死似乎仅限于血管腔。这些毒力实验的结果清楚地支持了以下假设：α-毒素和穿孔素溶血素O在坏疽性气体的病理学中具有协同作用。

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