Construction and virulence testing of a collagenase mutant of Clostridium perfringens
Construction and virulence testing of a collagenase mutant of Clostridium perfringens
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DOI：
10.1006/mpat.1999.0328
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发表时间：
2000-02-01
影响因子：
3.8
通讯作者：
Rood, JI
中科院分区：
文献类型：
--
作者：
Awad, MM;Ellemor, DM;Rood, JI
产气荚膜梭菌产生多种细胞外毒素和酶，包括由 colA 基因编码的细胞外胶原酶或 kappa 毒素。为了确定产生胶原酶的能力是否是产气荚膜梭菌引起的气性坏疽或梭菌性肌坏死病例中的重要毒力因子，通过同源重组构建了染色体 colA 突变体，并随后在小鼠肌坏死模型中测试了毒力。结果清楚地表明，产生胶原酶的能力的丧失不会改变突变体建立强毒感染的能力。相比之下，感染不能产生α-毒素的突变体会导致毒力显着下降。这些结果表明胶原酶不是产气荚膜梭菌介导的梭菌性肌坏死毒力的主要决定因素。 (C) 2000 年学术出版社。
Clostridium perfringens produces several extracellular toxins and enzymes, including an extracellular collagenase or kappa toxin that is encoded by the colA gene. To determine if the ability to produce collagenase was a significant virulence factor in cases of gas gangrene or clostridial myonecrosis that are caused by C. perfringens, a chromosomal colA mutant was constructed by homologous recombination and subsequently virulence tested in the mouse myonecrosis model. The results clearly indicate that loss of the ability to produce collagenase does not alter the ability of the mutant to establish a virulent infection. By contrast, infection with a mutant unable to produce alpha-toxin led to a marked decrease in virulence. These results indicate that collagenase is not a major determinant of virulence in C. perfringens-mediated clostridial myonecrosis. (C) 2000 Academic Press.