作为口腔扁平苔藓发病机制潜在促进因素的细菌胞外囊泡

IF 4.5 2区 医学 Q2 CELL BIOLOGY
Yu Gyung Kim, Hyo-Jin Song, Hyeon Ji Kim, Bo Kyung Joo, Jin-Hwa Cho, Won Jung, Sungil Jang, Song-Yi Choi, Heon-Jin Lee, Jin-Seok Byun, Do-Yeon Kim
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引用次数: 0

摘要

口腔扁平苔藓(OLP)是一种慢性炎症性疾病,其特点是细胞毒性 T 细胞的密集浸润导致角朊细胞死亡。角质细胞内的异常变化可能是 OLP 发病和进展的关键,但 OLP 的致病机制仍不确定。人类口腔微生物群由约 500 亿至 1000 亿个细菌实体组成,其中包括约 200 种优势细菌。这些细菌不断产生和释放胞外囊泡(EVs),在宿主与微生物的相互作用中发挥着重要作用。然而,这些细菌EVs对OLP进展的影响尚未完全阐明。在本研究中,通过全面的数据库分析和实验验证,我们观察到与非 OLP 组织相比,OLP 病变表现出炎症特征的升高和 STAT3 磷酸化的显著增加。值得注意的是,从主要牙周病原体牙龈卟啉单胞菌和放线菌中提取的 EVs 可诱导炎症反应并激活 STAT3 信号通路,这与在 OLP 中观察到的病理生理特征密切相关。这些结果突出了细菌EV在OLP发病机制中的潜在作用,并强调STAT3是这一过程中的关键介质。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Bacterial Extracellular Vesicles as Potential Promoting Factors for Oral Lichen Planus Pathogenesis.

Oral lichen planus (OLP) is a chronic inflammatory disease characterized by an intensive infiltration of cytotoxic T cells, which causes keratinocyte death. Abnormal changes within keratinocytes might be critical for OLP onset and progression, but the pathogenic mechanism of OLP is still uncertain. The human oral microbiota, consisting of approximately 50-100 billion bacterial entities, encompasses around 200 dominant bacterial species. These bacteria continuously produce and release extracellular vesicles (EVs), which play a significant role in host-microbe interactions. However, the impact of these bacterial EVs on the progression of OLP has not been fully elucidated. In this study, through comprehensive database analysis and experimental validation, we observed that OLP lesions exhibit elevated inflammatory signatures and significantly increased phosphorylation of STAT3 compared to non-OLP tissues. Notably, EVs derived from key periodontal pathogens, Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, were shown to induce an inflammatory response and activate STAT3 signaling pathways, closely mirroring the pathophysiological features observed in OLP. These results underscore the potential role of bacterial EVs in the pathogenesis of OLP and highlight STAT3 as a critical mediator in this process.

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来源期刊
Inflammation
Inflammation 医学-免疫学
CiteScore
9.70
自引率
0.00%
发文量
168
审稿时长
3.0 months
期刊介绍: Inflammation publishes the latest international advances in experimental and clinical research on the physiology, biochemistry, cell biology, and pharmacology of inflammation. Contributions include full-length scientific reports, short definitive articles, and papers from meetings and symposia proceedings. The journal''s coverage includes acute and chronic inflammation; mediators of inflammation; mechanisms of tissue injury and cytotoxicity; pharmacology of inflammation; and clinical studies of inflammation and its modification.
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