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SufA – a bacterial enzyme that cleaves fibrinogen and blocks fibrin network formation

机译:SUFA - 一种切割纤维蛋白原和阻断纤维蛋白网络形成的细菌酶

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Finegoldia magna is a member of the normal human bacterial flora on the skin and other non-sterile body surfaces, but this anaerobic coccus is also an important opportunistic pathogen. SufA was the first F. magna proteinase to be isolated and characterized. Many bacterial pathogens interfere with different steps of blood coagulation, and here we describe how purified SufA efficiently and specifically cleaves fibrinogen in human plasma. SufA is both secreted by F. magna and associated with the bacterial surface. Successful gene targeting has previously not been performed in anaerobic cocci, but in order to study the role of the SufA that is present at the bacterial surface, we constructed an F. magna mutant that expresses a truncated SufA lacking proteolytic activity. In contrast to wild-type bacteria that delayed the coagulation of human plasma, mutant bacteria had no such effect. Wild-type and mutant bacteria adhered to keratinocytes equally well, but in a plasma environment only wild-type bacteria blocked the formation of fibrin networks surrounding adherent bacteria. The effective cleavage of fibrinogen by SufA suggests that the interference with fibrin network formation represents an adaptive mechanism of F. magna with potential implications also for pathogenicity.
机译:FineGoldia Magna是皮肤和其他非无菌体面的正常人体细菌菌群的成员,但这种厌氧Coccus也是一个重要的机会理性病原体。 SUFA是第一个被隔离和表征的MAMMA蛋白酶。许多细菌病原体干扰了血液凝固的不同步骤,在这里,我们描述了如何有效地纯化的SUFA,并且具体地切割人血浆中的纤维蛋白原。 SUFA既由F.MAMMA分泌并与细菌表面相关。以前未在厌氧COCCC上进行成功的基因靶向,但为了研究在细菌表面存在的SUFA的作用,我们构建了一种表达缺乏蛋白水解活性的截短的SUFA的F.MAGA突变体。与延迟人血浆凝血的野生型细菌相比,突变细菌没有这种作用。野生型和突变细菌同样粘附在角质形成细胞,但在血浆环境中只有野生型细菌阻断纤维蛋白网络周围围绕着粘附细菌的形成。 SUFA的纤维蛋白原的有效切割表明,对纤维蛋白网络形成的干扰是F.MMANA的自适应机制,其潜在影响也用于致病性。

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