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变形链球菌的血清型特异性多糖有助于心内膜炎的感染性。

Serotype-specific polysaccharide of Streptococcus mutans contributes to infectivity in endocarditis.

作者信息

Nagata E, Okayama H, Ito H-O, Yamashita Y, Inoue M, Oho T

机构信息

Department of Preventive Dentistry, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.

出版信息

Oral Microbiol Immunol. 2006 Dec;21(6):420-3. doi: 10.1111/j.1399-302X.2006.00317.x.

Abstract

Streptococcus mutans and other viridans streptococci have been implicated as major etiological agents of infective endocarditis. The serotype-specific rhamnose-glucose polysaccharide (RGP) of S. mutans has several biological functions that appear to be essential for the induction of infective endocarditis. The aim of this study was to examine the contribution of RGP to the infectivity of S. mutans in infective endocarditis using a rat model. The RGP-defective mutant of S. mutans showed reduced ability to induce infective endocarditis compared to the parental strain. The ability of S. mutans to induce infective endocarditis was not consistent with the binding capacity of the organism to extracellular matrix proteins. The results suggest that S. mutans containing whole RGP is more virulent than the RGP-defective mutant, and the RGP has an important role for the induction of infective endocarditis by S. mutans.

摘要

变形链球菌和其他草绿色链球菌被认为是感染性心内膜炎的主要病原体。变形链球菌的血清型特异性鼠李糖 - 葡萄糖多糖(RGP)具有多种生物学功能,这些功能似乎对于感染性心内膜炎的诱发至关重要。本研究的目的是使用大鼠模型研究RGP对变形链球菌在感染性心内膜炎中感染性的贡献。与亲本菌株相比,变形链球菌的RGP缺陷型突变体诱导感染性心内膜炎的能力降低。变形链球菌诱导感染性心内膜炎的能力与该生物体与细胞外基质蛋白的结合能力不一致。结果表明,含有完整RGP的变形链球菌比RGP缺陷型突变体更具毒性,并且RGP在变形链球菌诱发感染性心内膜炎中起重要作用。

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