Role of dentilisin in Treponema denticola epithelial cell layer penetration
Role of dentilisin in Treponema denticola epithelial cell layer penetration
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DOI：
10.1016/j.resmic.2003.08.001
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发表时间：
2003-11-01
影响因子：
2.6
通讯作者：
Kuramitsu, HK
中科院分区：
文献类型：
--
作者：
Chi, B;Qi, M;Kuramitsu, HK
齿垢密螺旋体是一种与牙周病有关的口腔厌氧螺旋体。胰凝乳蛋白酶样蛋白酶牙本质蛋白酶（PrtP）是齿垢锥虫的重要毒力因子。在这项研究中，我们研究的作用，牙本质素在T齿垢上皮细胞单层渗透比较野生型和prtP突变。野生型齿垢毛癣菌可以破坏跨上皮电阻（TER），并基本上穿透HEp-2细胞层。prtP突变体仅轻微改变单层，并以非常低的数量穿透Hep-2层。野生型齿垢锥虫的膜部分能够补充单层渗透的prtP突变体，而突变体的可比部分没有这样的效果。免疫荧光研究表明，野生型齿垢毛癣菌可能通过降解紧密连接蛋白（如ZO-1）来改变TER。细胞毒性不是TER破坏的主要因素。野生型齿垢锥虫的外膜囊泡（OMV）也破坏了上皮屏障功能，并穿透上皮层。两者合计，这些结果表明，齿垢锥虫穿透上皮细胞单层，通过改变细胞的紧密连接。(C)2003年，Elsevier SAS科学与医学版。All rights reserved.
Treponema denticola is an oral anaerobic spirochete implicated in periodontal diseases. The chymotrypsin-like protease, dentilisin (PrtP), has been suggested to be an important virulence factor of T denticola. In this study, we examined the role of dentilisin in T denticola epithelial monolayer penetration by comparing the wild type and prtP mutant. Wild-type T denticola can disrupt transepithelial resistance (TER) and substantially penetrate the HEp-2 cell layer. The prtP mutant altered the monolayer only slightly and penetrated the Hep-2 layer in very low numbers. The membrane fraction of wild-type T denticola is able to complement the prtP mutant in monolayer penetration, while the comparable fraction from the mutant has no such effect. Immunofluorescence studies suggested that wild-type T denticola altered the TER by likely degrading the tight junctional proteins such as ZO-1. Cytotoxicity was not a major factor in the disruption of TER. The outer membrane vesicles (OMVs) of wild-type T denticola also disrupted epithelial barrier function and penetrated the epithelial layers. Taken together, these results suggest that T denticola penetrates the epithelial cell monolayers; by altering cellular tight junctions. (C) 2003 Editions scientifiques et medicales Elsevier SAS. All rights reserved.