Disruption of epithelial barrier and impairment of cellular function by Porphyromonas gingivalis
Disruption of epithelial barrier and impairment of cellular function by Porphyromonas gingivalis
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DOI：
10.2741/2363
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发表时间：
2007-05-01
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影响因子：
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通讯作者：
Amano, Atsuo
中科院分区：
文献类型：
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作者：
Amano, Atsuo
牙龈卟啉单胞菌是一种主要的牙周病原菌，它表达许多与牙周炎发病相关的潜在毒力因子。牙龈上皮细胞自发地暴露在细菌的攻击下，其功能是防止细菌入侵更深的组织。牙龈假单胞菌菌毛是调节机体与宿主组织相互作用的关键因素，因为它们促进了细菌对目标部位的黏附和入侵。菌毛能够与人唾液成分、细胞外基质蛋白和共生菌结合，同时也能与细胞内的α5β1整合素紧密结合。在与α5β1整合素黏附后，牙龈假单胞菌被细胞伪足捕获，这使得内陷能够通过肌动蛋白介导的途径进行。据报道，这种侵袭性事件需要宿主细胞动力素、肌动蛋白纤维、微管和脂筏。在穿过上皮屏障后，细胞内的病原体会损害细胞功能。根据FIMA基因编码每个菌毛亚基的多样性，菌毛被分为6种类型(I-V和Ib型)，并且发现含有II型菌毛的细胞内牙龈假单胞菌能够明显降解整合素相关信号分子、Paxlin和粘着斑激酶，从而使细胞无法迁移和增殖。这些事件被认为整合了细菌在牙周组织中持续存在的策略。
Porphyromonas gingivalis is a predominant periodontal pathogen that expresses a number of potential virulence factors involved in the pathogenesis of periodontitis. Gingival epithelial cells are spontaneously exposed to bacterial attacks and function to prevent invasion by bacteria into deeper tissues. P. gingivalis fimbriae are a critical factor for mediation of interaction of the organism with host tissues, as they promote both bacterial adhesion to and invasion of targeted sites. Fimbriae are capable of binding to human salivary components, extracellular matrix proteins, and commensal bacteria, while they also strongly adhere to cellular alpha 5 beta 1-integrin. Following adhesion to alpha 5 beta 1-integrin, P. gingivalis is captured by cellular pseudopodia, which enables invagination through an actin-mediated pathway. The invasive event has been reported to require host cellular dynamin, actin fibers, microtubules, and lipid rafts. Following passage through the epithelial barrier, the intracellular pathogen impairs cellular function. Fimbriae are classified into 6 genotypes (types I to V and Ib) based on the diversity of the fimA genes encoding each fimbria subunit, and intracellular P. gingivalis with type II fimbriae has been found to clearly degrade integrin-related signaling molecules, paxillin, and focal adhesion kinase, which disables cellular migration and proliferation. These events are considered to integrate the bacterial strategy for persistence in periodontal tissues.