The presence of bacteria within tissue provides insights into the pathogenesis of oral lichen planus.
The presence of bacteria within tissue provides insights into the pathogenesis of oral lichen planus.
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DOI：
10.1038/srep29186
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发表时间：
2016-07-07
影响因子：
4.6
通讯作者：
Choi Y
中科院分区：
文献类型：
--
作者：
Choi YS;Kim Y;Yoon HJ;Baek KJ;Alam J;Park HK;Choi Y
口腔扁平苔藓（OLP）是一种病因不明的慢性T细胞介导的皮肤粘膜疾病。虽然已经考虑了各种抗原，但实际上触发T细胞炎症反应的是未知的。在本研究中，我们提出，细胞内细菌存在于组织内触发T细胞浸润，并提供靶抗原。对OLP（n = 36）和正常（n = 10）口腔粘膜组织切片进行原位杂交，使用靶向细菌16 S rRNA基因的通用探针和抗CD 3、抗CD 4、抗CD 8和抗巨噬细胞特异性抗体的免疫组织化学。口腔扁平苔藓组织的上皮和固有层中细菌含量丰富，与浸润的CD 3+、CD 4+和CD 8+细胞水平呈正相关。此外，在浸润的T细胞内检测到细菌。来自OLP患者（n = 13）和对照受试者（n = 11）的粘膜微生物群的焦磷酸测序分析揭示了OLP病变中链球菌的减少和牙龈炎/牙周炎相关细菌的增加。使用选定的细菌物种，我们证明了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CXCL 10和CCL 5的产生。我们的研究结果提供了深入了解OLP的发病机制。
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.