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齿垢密螺旋体ATCC 35405生物膜形成的遗传分析

Genetic analysis of Treponema denticola ATCC 35405 biofilm formation.

作者信息

Vesey Peter M, Kuramitsu Howard K

机构信息

Department of Oral Biology, State University of New York at Buffalo, 3435 Main Street, Buffalo, NY 14214-3092, USA.

出版信息

Microbiology (Reading). 2004 Jul;150(Pt 7):2401-2407. doi: 10.1099/mic.0.26816-0.

Abstract

Treponema denticola is a major aetiological organism implicated in periodontal disease. The interaction of T. denticola with other oral bacteria, in particular Porphyromonas gingivalis, in biofilm formation is thought to be an important step in the onset of periodontal disease. The interaction between T. denticola and P. gingivalis has been examined using a panel of T. denticola mutants and their effects on mixed biofilm formation tested in a static biofilm model. T. denticola ATCC 35405 did not form detectable biofilms on various inert surfaces. However, the spirochaete was demonstrated to form a biofilm with preattached P. gingivalis 381. T. denticola cfpA, which lacks the cytoplasmic filament, was unable to produce a mixed biofilm with P. gingivalis. A T. denticola flgE mutant which lacks the flagella hook protein and is therefore non-motile displayed a reduced, but readily detectable, ability to form a mixed biofilm as did the T. denticola mutant which does not possess the major outer sheath protein (Msp). The T. denticola lrrA mutant was only moderately defective in forming mixed biofilms with P. gingivalis. However, the T. denticola methyl-accepting chemotaxis protein (DmcA) did not appear to play a major role in mixed biofilm formation. In contrast, T. denticola lacking the PrtP protein for prolyl-phenylalanine-specific protease, showed an increased ability to form mixed biofilms and a prolonged viability in the biofilm.

摘要

齿垢密螺旋体是与牙周病相关的主要病原菌。齿垢密螺旋体与其他口腔细菌,尤其是牙龈卟啉单胞菌在生物膜形成中的相互作用被认为是牙周病发病的重要步骤。已使用一组齿垢密螺旋体突变体研究了齿垢密螺旋体与牙龈卟啉单胞菌之间的相互作用,并在静态生物膜模型中测试了它们对混合生物膜形成的影响。齿垢密螺旋体ATCC 35405在各种惰性表面上未形成可检测到的生物膜。然而,已证明这种螺旋体可与预先附着的牙龈卟啉单胞菌381形成生物膜。缺乏细胞质丝的齿垢密螺旋体cfpA无法与牙龈卟啉单胞菌产生混合生物膜。缺乏鞭毛钩蛋白因而无运动能力的齿垢密螺旋体flgE突变体形成混合生物膜的能力有所降低,但仍易于检测到,不具有主要外鞘蛋白(Msp)的齿垢密螺旋体突变体也是如此。齿垢密螺旋体lrrA突变体在与牙龈卟啉单胞菌形成混合生物膜方面仅存在中度缺陷。然而,齿垢密螺旋体甲基接受趋化蛋白(DmcA)似乎在混合生物膜形成中不起主要作用。相反,缺乏脯氨酰 - 苯丙氨酸特异性蛋白酶的PrtP蛋白的齿垢密螺旋体显示出形成混合生物膜的能力增强,并且在生物膜中的生存能力延长。

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