PDF(Pubmed)
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.
摘要：
连翘坦菌,与严重牙周炎有关的“红色复合物”细菌的成员，采用各种生存策略和毒力因子与宿主相互作用。它作为口腔生物膜中的晚期定殖者而茁壮成长，依靠其独特的持久性适应机制。其存活的关键是9型蛋白质分泌系统和蛋白质的O-糖基化，对于宿主相互作用和免疫逃避至关重要。连翘毒力因子,包括唾液酸酶和蛋白酶,通过降解宿主糖蛋白和蛋白质来促进其致病性，分别。此外，细胞表面糖蛋白如S层和BspA调节宿主反应和细菌粘附，影响定植和组织浸润。外膜囊泡和脂多糖进一步诱导炎症反应，导致牙周组织破坏.与特定宿主细胞类型的相互作用，包括上皮细胞,多形核白细胞巨噬细胞，和间充质基质细胞，突出连翘致病性的多面性。值得注意的是,它可以侵入上皮细胞并损害PMN功能，促进失调的炎症和细菌存活。与牙周炎相关的牙龈卟啉单胞菌的比较研究揭示了蛋白酶活性和免疫调节的差异，提示在疾病进展中的不同作用。连翘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的潜力强调了其在牙周病发病机理中的重要性。然而,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需要进一步研究。翻译研究数据的挑战来自口腔微生物组和生物膜动力学的复杂性，需要进行全面的研究以阐明其在牙周炎管理中的临床相关性和治疗意义。
