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组织内细菌的存在为口腔扁平苔藓的发病机制提供了线索。

The presence of bacteria within tissue provides insights into the pathogenesis of oral lichen planus.

机构信息

Departments of Oral Microbiology and Immunology, School of Dentistry and Dental Research Institute, Seoul National University, 101 Daehak-ro, Jongno-gu, Seoul 03080, Republic of Korea.

Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, 101 Daehak-ro, Jongno-gu, Seoul 03080, Republic of Korea.

出版信息

Sci Rep. 2016 Jul 7;6:29186. doi: 10.1038/srep29186.

DOI:10.1038/srep29186
PMID:27383402
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4935860/
Abstract

Oral lichen planus (OLP) is a chronic T cell-mediated mucocutaneous disease of unknown etiopathogenesis. Although various antigens have been considered, what actually triggers the inflammatory response of T cells is unknown. In the present study, we propose that intracellular bacteria present within tissues trigger T cell infiltration and provide target antigens. Sections of OLP (n = 36) and normal (n = 10) oral mucosal tissues were subjected to in situ hybridization using a universal probe targeting the bacterial 16S rRNA gene and immunohistochemistry with anti-CD3, anti-CD4, anti-CD8, and anti-macrophage-specific antibodies. Bacteria were abundant throughout the epithelium and the lamina propria of OLP tissues, which exhibited positive correlations with the levels of infiltrated CD3(+), CD4(+), and CD8(+) cells. Furthermore, bacteria were detected within the infiltrated T cells. Pyrosequencing analysis of the mucosal microbiota from OLP patients (n = 13) and control subjects (n = 11) revealed a decrease in Streptococcus and increases in gingivitis/periodontitis-associated bacteria in OLP lesions. Using the selected bacterial species, we demonstrated that certain oral bacteria damage the epithelial physical barrier, are internalized into epithelial cells or T cells, and induce production of T cell chemokines CXCL10 and CCL5. Our findings provide insights into the pathogenesis of OLP.

摘要

口腔扁平苔藓(OLP)是一种病因不明的慢性 T 细胞介导的黏膜疾病。虽然已经考虑了各种抗原,但实际上触发 T 细胞炎症反应的原因尚不清楚。在本研究中,我们提出组织内存在的内源性细菌触发 T 细胞浸润并提供靶抗原。使用针对细菌 16S rRNA 基因的通用探针对 OLP(n=36)和正常(n=10)口腔黏膜组织进行原位杂交,并使用抗 CD3、抗 CD4、抗 CD8 和抗巨噬细胞特异性抗体进行免疫组织化学染色。细菌在 OLP 组织的整个上皮和固有层中大量存在,与浸润的 CD3(+)、CD4(+)和 CD8(+)细胞水平呈正相关。此外,在浸润的 T 细胞内也检测到了细菌。对 OLP 患者(n=13)和对照组(n=11)的黏膜微生物组进行焦磷酸测序分析显示,OLP 病变中链球菌减少,与牙龈炎/牙周炎相关的细菌增加。使用选定的细菌物种,我们证明某些口腔细菌破坏上皮物理屏障,被内化到上皮细胞或 T 细胞中,并诱导 T 细胞趋化因子 CXCL10 和 CCL5 的产生。我们的研究结果为 OLP 的发病机制提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a6/4935860/b0444d58ce88/srep29186-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a6/4935860/a7947a48f245/srep29186-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a6/4935860/0c16a07de788/srep29186-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a6/4935860/e6e4e02fc124/srep29186-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a6/4935860/f688578678bd/srep29186-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a6/4935860/016e451ac180/srep29186-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a6/4935860/b0444d58ce88/srep29186-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a6/4935860/a7947a48f245/srep29186-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a6/4935860/0c16a07de788/srep29186-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a6/4935860/e6e4e02fc124/srep29186-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a6/4935860/f688578678bd/srep29186-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a6/4935860/016e451ac180/srep29186-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a6/4935860/b0444d58ce88/srep29186-f6.jpg

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