The intriguing strategies of Tannerella forsythia's host interaction.

IF 3 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Frontiers in oral health Pub Date : 2024-05-30 eCollection Date: 2024-01-01 DOI:10.3389/froh.2024.1434217
Christina Schäffer, Oleh Andrukhov
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Abstract

Tannerella forsythia, a member of the "red complex" bacteria implicated in severe periodontitis, employs various survival strategies and virulence factors to interact with the host. It thrives as a late colonizer in the oral biofilm, relying on its unique adaptation mechanisms for persistence. Essential to its survival are the type 9 protein secretion system and O-glycosylation of proteins, crucial for host interaction and immune evasion. Virulence factors of T. forsythia, including sialidase and proteases, facilitate its pathogenicity by degrading host glycoproteins and proteins, respectively. Moreover, cell surface glycoproteins like the S-layer and BspA modulate host responses and bacterial adherence, influencing colonization and tissue invasion. Outer membrane vesicles and lipopolysaccharides further induce inflammatory responses, contributing to periodontal tissue destruction. Interactions with specific host cell types, including epithelial cells, polymorphonuclear leukocytes macrophages, and mesenchymal stromal cells, highlight the multifaceted nature of T. forsythia's pathogenicity. Notably, it can invade epithelial cells and impair PMN function, promoting dysregulated inflammation and bacterial survival. Comparative studies with periodontitis-associated Porphyromonas gingivalis reveal differences in protease activity and immune modulation, suggesting distinct roles in disease progression. T. forsythia's potential to influence oral antimicrobial defense through protease-mediated degradation and interactions with other bacteria underscores its significance in periodontal disease pathogenesis. However, understanding T. forsythia's precise role in host-microbiome interactions and its classification as a keystone pathogen requires further investigation. Challenges in translating research data stem from the complexity of the oral microbiome and biofilm dynamics, necessitating comprehensive studies to elucidate its clinical relevance and therapeutic implications in periodontitis management.

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连翘丹那菌与宿主相互作用的有趣策略。
连翘丹那菌是与严重牙周炎有关的 "红色复合菌 "的一种,它采用各种生存策略和毒力因子与宿主相互作用。它是口腔生物膜中的晚期定植菌,依靠其独特的适应机制得以生存。其生存的关键是 9 型蛋白质分泌系统和蛋白质的 O 型糖基化,这对与宿主互动和逃避免疫至关重要。连翘的致病因子,包括硅糖苷酶和蛋白酶,分别通过降解宿主糖蛋白和蛋白质促进其致病性。此外,细胞表面糖蛋白(如 S 层和 BspA)可调节宿主反应和细菌粘附性,影响定植和组织侵袭。外膜囊泡和脂多糖进一步诱发炎症反应,造成牙周组织破坏。连翘与特定宿主细胞类型(包括上皮细胞、多形核白细胞、巨噬细胞和间质基质细胞)的相互作用凸显了连翘致病的多面性。值得注意的是,它可以侵入上皮细胞,损害多核白细胞的功能,促进炎症失调和细菌存活。与牙周炎相关的牙龈卟啉单胞菌(Porphyromonas gingivalis)的比较研究显示,连翘在蛋白酶活性和免疫调节方面存在差异,这表明它在疾病进展中扮演着不同的角色。连翘菌可能通过蛋白酶介导的降解和与其他细菌的相互作用影响口腔抗菌防御,这凸显了它在牙周病发病机制中的重要性。然而,要了解连翘在宿主-微生物组相互作用中的确切作用及其作为关键病原体的分类还需要进一步的研究。口腔微生物组和生物膜动态的复杂性给研究数据的转化带来了挑战,因此有必要进行综合研究,以阐明其在牙周炎治疗中的临床相关性和治疗意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
3.30
自引率
0.00%
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0
审稿时长
13 weeks
期刊最新文献
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