Effect of Treponema Denticola Infection on Epithelial Cells.

IF 0.5 Q4 DENTISTRY, ORAL SURGERY & MEDICINE
Bulletin of Tokyo Dental College Pub Date : 2022-03-08 Epub Date: 2022-02-15 DOI:10.2209/tdcpublication.2021-0037
Eitoyo Kokubu, Yuichiro Kikuchi, Kazuko Okamoto-Shibayama, Kazuyuki Ishihara
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引用次数: 0

Abstract

Chronic periodontitis is an infectious disease caused by periodontopathic bacteria in subgingival plaque. One major pathogen of this disease, Treponema denticola, has several virulence factors, including a major surface protein (Msp) and the surface protease dentilisin. The cytopathic effects of periodontopathic bacteria on epithelial cells disrupt the integrity of the barrier junction, resulting in the inflammation of periodontal tissue. The aim of this study was to investigate the effect of T. denticola virulence factors dentilisin and Msp on epithelial cells. The effects of T. denticola wild-type, Msp-mutant, and dentilisin-mutant strains on the contact junction in Madin-Darby canine kidney epithelial cells was evaluated based on ohmic values. Cultured oral carcinoma epithelial cells were scratched and exposed to the selected T. denticola strains and cell migration determined. Subsequent degradation of adherence proteins and proteins in the contact junctions was evaluated. Dissociation of cell contact junctions was detected in cells infected with wild-type T. denticola approximately 30 min after infection, but not in those exposed to the mutants. Inhibition of migration was observed in the wild-type and Msp-deficient mutants. The adherent proteins focal adhesion kinase, ZO-1, and paxillin were hydrolyzed by infection with the wild-type and Msp mutants. These results indicate that T. denticola disrupts the function of epithelial cells by hydrolyzing proteins at the intercellular junction and inhibiting healing of epithelial cells via hydrolyzed proteins associated with focal adhesion; Msp was also associated with these effects.

密螺旋体感染对上皮细胞的影响。
慢性牙周炎是由牙龈下菌斑中的牙周病细菌引起的一种感染性疾病。这种疾病的一个主要病原体,牙密螺旋体,有几个毒力因子,包括一个主要的表面蛋白(Msp)和表面蛋白酶牙lisin。牙周病细菌对上皮细胞的细胞病变作用破坏了屏障连接的完整性,导致牙周组织的炎症。本研究旨在探讨牙齿田鼠毒力因子牙lisin和Msp对上皮细胞的影响。利用欧姆值评价了野生型、msp突变型和牙胶素突变株对Madin-Darby犬肾上皮细胞接触连接的影响。将培养的口腔癌上皮细胞划伤,暴露于所选的牙齿菌菌株中,观察细胞迁移情况。随后的降解粘附蛋白和蛋白质的接触连接进行了评估。在感染野生型齿状螺旋体的细胞中,在感染后约30分钟检测到细胞接触连接的解离,但在暴露于突变体的细胞中没有检测到。在野生型和msp缺陷突变体中观察到迁移受到抑制。通过感染野生型和Msp突变体,可以水解黏附蛋白focal adhesion kinase、ZO-1和paxillin。这些结果表明,齿状霉通过水解细胞间连接处的蛋白来破坏上皮细胞的功能,并通过与局灶黏附相关的水解蛋白来抑制上皮细胞的愈合;Msp也与这些影响有关。
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来源期刊
Bulletin of Tokyo Dental College
Bulletin of Tokyo Dental College DENTISTRY, ORAL SURGERY & MEDICINE-
CiteScore
0.90
自引率
0.00%
发文量
15
期刊介绍: The bulletin of Tokyo Dental collegue is principally for the publication of original contributions to multidisciplinary research in dentistry.
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