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

机译:SufA –一种细菌酶可裂解纤维蛋白原并阻断纤维蛋白网络的形成

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摘要

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:大花是皮肤和其他非无菌体表上正常人类细菌菌群的成员,但这种厌氧球菌也是重要的机会病原体。 SufA是第一个被分离和鉴定的F. magna蛋白酶。许多细菌性病原体会干扰血液凝固的不同步骤,在这里我们描述了纯化的SufA如何有效且特异性地裂解人血浆中的纤维蛋白原。 SufA都由巨乳念珠菌分泌并与细菌表面有关。以前尚未在厌氧球菌中成功进行基因靶向,但是为了研究存在于细菌表面的SufA的作用,我们构建了F.magna突变体,该突变体表达了缺乏蛋白水解活性的截短的SufA。与延迟人类血浆凝结的野生型细菌相反,突变细菌没有这种作用。野生型和突变型细菌同样能很好地粘附于角质形成细胞,但在血浆环境中,只有野生型细菌才能阻止围绕粘附性细菌的血纤蛋白网络的形成。 SufA对血纤蛋白原的有效切割表明,对血纤蛋白网络形成的干扰代表了大镰刀菌的一种适应机制,对致病性也有潜在影响。

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