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感染诱导脂多糖和肽聚糖穿透牙龈上皮。

Infection Induces Lipopolysaccharide and Peptidoglycan Penetration Through Gingival Epithelium.

作者信息

Takeuchi Hiroki, Nakamura Eriko, Yamaga Shunsuke, Amano Atsuo

机构信息

Department of Preventive Dentistry, Osaka University Dental Hospital, Suita, Japan.

Department of Preventive Dentistry, Graduate School of Dentistry, Osaka University, Suita, Japan.

出版信息

Front Oral Health. 2022 Feb 8;3:845002. doi: 10.3389/froh.2022.845002. eCollection 2022.

Abstract

Periodontal diseases initiate on epithelial surfaces of the subgingival compartment, while the gingival epithelium functions as an epithelial barrier against microbial infection and orchestrates immune responses. is a major pathogen of periodontal diseases and has an ability to penetrate the epithelial barrier. To assess the molecular basis of gingival epithelial barrier dysfunction associated with , we newly developed a three-dimensional multilayered tissue model of gingival epithelium with gene manipulation. Using this novel approach, gingipains including Arg- or Lys-specific cysteine proteases were found to specifically degrade junctional adhesion molecule 1 and coxsackievirus and adenovirus receptor in the tissue model, leading to increased permeability for lipopolysaccharide, peptidoglycan, and gingipains. This review summarizes the strategy used by to disable the epithelial barrier by disrupting specific junctional adhesion molecules.

摘要

牙周疾病始发于龈下区域的上皮表面,而牙龈上皮作为抵御微生物感染的上皮屏障,并协调免疫反应。[某种细菌]是牙周疾病的主要病原体,具有穿透上皮屏障的能力。为了评估与[该细菌]相关的牙龈上皮屏障功能障碍的分子基础,我们新开发了一种可进行基因操作的牙龈上皮三维多层组织模型。使用这种新方法,发现包括精氨酸或赖氨酸特异性半胱氨酸蛋白酶在内的[该细菌的]牙龈蛋白酶能在组织模型中特异性降解连接粘附分子1以及柯萨奇病毒和腺病毒受体,导致脂多糖、肽聚糖和牙龈蛋白酶的通透性增加。本综述总结了[该细菌]通过破坏特定连接粘附分子来破坏上皮屏障的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d9/8861192/3d74ddba9ce4/froh-03-845002-g0001.jpg

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