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产气荚膜梭菌胶原酶突变体的构建及毒力测试

Construction and virulence testing of a collagenase mutant of Clostridium perfringens.

作者信息

Awad M M, Ellemor D M, Bryant A E, Matsushita O, Boyd R L, Stevens D L, Emmins J J, Rood J I

机构信息

Bacterial Pathogenesis Research Group, Department of Microbiology, Clayton, 3800, Australia.

出版信息

Microb Pathog. 2000 Feb;28(2):107-17. doi: 10.1006/mpat.1999.0328.

Abstract

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.

摘要

产气荚膜梭菌可产生多种细胞外毒素和酶,包括由colA基因编码的一种细胞外胶原酶或κ毒素。为了确定产生胶原酶的能力是否是由产气荚膜梭菌引起的气性坏疽或梭菌性肌坏死病例中的一个重要毒力因子,通过同源重组构建了一个染色体colA突变体,并随后在小鼠肌坏死模型中进行了毒力测试。结果清楚地表明,产生胶原酶能力的丧失并不改变突变体建立毒性感染的能力。相比之下,感染不能产生α毒素的突变体导致毒力显著降低。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中毒力的主要决定因素。

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