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变形链球菌对纤溶酶原的激活作用。

Activation of plasminogen by Streptococcus mutans.

作者信息

Jones Micheala N, Holt Robert G

机构信息

Department of Microbiology, Meharry Medical College, Nashville, TN 37208, USA.

出版信息

Biochem Biophys Res Commun. 2004 Sep 10;322(1):37-41. doi: 10.1016/j.bbrc.2004.07.077.

Abstract

Streptococcus mutans, a member of the viridans streptococci, is the etiologic agent of dental caries and is also a causative agent of subacute infective endocarditis. The generation of proteolytic molecules, such as plasmin, may be important in the pathogenesis of endocarditis caused by S. mutans. In this study, we demonstrate that S. mutans cells have the ability to bind and activate plasminogen to plasmin. Incubation of S. mutans cells with plasminogen was found to be sufficient for the activation of plasminogen, which suggests the presence of an endogenously produced plasminogen activator. The plasmin activity generated by S. mutans cells was shown to be inhibited by epsilon-aminocaproic acid, lysine, aprotinin, and alpha(2)-macroglobulin. We also show that S. mutans cells have the ability to bind and activate plasminogen from human plasma as well as human serum. The plasmin activity generated on the surface of S. mutans cells could degrade the extracellular matrix molecule, fibronectin.

摘要

变形链球菌是草绿色链球菌属的一员,是龋齿的病原体,也是亚急性感染性心内膜炎的致病因子。蛋白水解分子(如纤溶酶)的产生可能在变形链球菌引起的心内膜炎发病机制中起重要作用。在本研究中,我们证明变形链球菌细胞具有将纤溶酶原结合并激活为纤溶酶的能力。发现将变形链球菌细胞与纤溶酶原一起孵育足以激活纤溶酶原,这表明存在内源性产生的纤溶酶原激活剂。变形链球菌细胞产生的纤溶酶活性被ε-氨基己酸、赖氨酸、抑肽酶和α2-巨球蛋白抑制。我们还表明,变形链球菌细胞具有结合并激活来自人血浆以及人血清的纤溶酶原的能力。变形链球菌细胞表面产生的纤溶酶活性可降解细胞外基质分子纤连蛋白。

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