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首页> 外文期刊>Infection and immunity >Effects of Clostridium perfringens Alpha-Toxin (PLC) and Perfringolysin O (PFO) on Cytotoxicity to Macrophages, on Escape from the Phagosomes of Macrophages, and on Persistence of C. perfringens in Host Tissues
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Effects of Clostridium perfringens Alpha-Toxin (PLC) and Perfringolysin O (PFO) on Cytotoxicity to Macrophages, on Escape from the Phagosomes of Macrophages, and on Persistence of C. perfringens in Host Tissues

机译：产气荚膜梭菌α毒素（PLC）和产气荚膜溶素O（PFO）对巨噬细胞的细胞毒性，逃脱巨噬细胞吞噬作用以及对产气荚膜梭菌在宿主组织中的持久性的影响

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Clostridium perfringens is the most common cause of clostridial myonecrosis (gas gangrene). Polymorphonuclear cells (PMNs) appear to play only a minor role in preventing the onset of myonecrosis in a mouse animal model of the disease (unpublished results). However, the importance of macrophages in the host defense against C. perfringens infections is still unknown. Two membrane-active toxins produced by the anaerobic C. perfringens, alpha-toxin (PLC) and perfringolysin O (PFO), are thought to be important in the pathogenesis of gas gangrene and the lack of phagocytic cells at the site of infection. Therefore, C. perfringens mutants lacking PFO and PLC were examined for their relative cytotoxic effects on macrophages, their ability to escape the phagosome of macrophages, and their persistence in mouse tissues. C. perfringens survival in the presence of mouse peritoneal macrophages was dependent on both PFO and PLC. PFO was shown to be the primary mediator of C. perfringens-dependent cytotoxicity to macrophages. Escape of C. perfringens cells from phagosomes of macrophage-like J774-33 cells and mouse peritoneal macrophages was mediated by either PFO or PLC, although PFO seemed to play a more important role in escape from the phagosome in peritoneal macrophages. At lethal doses (109) of bacteria only PLC was necessary for the onset of myonecrosis, while at sublethal doses (106) both PFO and PLC were necessary for survival of C. perfringens in mouse muscle tissue. These results suggest PFO-mediated cytotoxicity toward macrophages and the ability to escape macrophage phagosomes may be important factors in the ability of C. perfringens to survive in host tissues when bacterial numbers are low relative to those of phagocytic cells, e.g., early in an infection.
机译：产气荚膜梭状芽孢杆菌是造成梭菌性肌坏死（坏疽性气体）的最常见原因。在该疾病的小鼠动物模型中，多形核细胞（PMN）似乎仅在预防骨髓坏死发作中起次要作用（未发表的结果）。但是，巨噬细胞在宿主防御 C的重要性。产气荚膜炎感染仍然未知。厌氧菌 C产生的两种膜活性毒素。产气荚膜炎，α-毒素（PLC）和产气荚膜溶血素O（PFO）被认为在气体坏疽的发病机理和感染部位吞噬细胞的缺乏方面很重要。因此， C。研究了缺乏PFO和PLC的perfringens 突变体对巨噬细胞的相对细胞毒性作用，它们逃避巨噬细胞吞噬体的能力以及它们在小鼠组织中的持久性。 C。小鼠腹膜巨噬细胞存在时，perfringens 的存活取决于PFO和PLC。 PFO被证明是C的主要介体。产气荚膜杆菌对巨噬细胞的依赖性细胞毒性。 C的转义符。 PFO或PLC介导了巨噬细胞样J774-33细胞和小鼠腹膜巨噬细胞吞噬物中的perfringens 细胞，尽管PFO在逃脱腹膜巨噬细胞吞噬体中起着更重要的作用。在致死剂量（10 9 ）的细菌中，仅需PLC才可发生坏死，而在致死剂量（10 6 ）时，PFO和PLC均需用于生存。 C。小鼠肌肉组织中的perfringens 。这些结果表明PFO介导的对巨噬细胞的细胞毒性和逃避巨噬细胞吞噬体的能力可能是 C能力的重要因素。当细菌数量相对于吞噬细胞的细菌数量低时，例如在感染的早期，产气荚膜杆菌可以在宿主组织中存活。

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