Liu Jia, Xia Wenhui, Cheng Juehua, Geng Yanlin, Li Weiping, Fan Yuan
Department of Oral Mucosal Diseases, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing, China.
State Key Laboratory Cultivation Base of Research, Prevention and Treatment for Oral Diseases, Nanjing, China.
Front Cell Infect Microbiol. 2025 Apr 29;15:1585020. doi: 10.3389/fcimb.2025.1585020. eCollection 2025.
Microbial dysbiosis links to mucosal immune dysregulation, but the specific bacterial contributions to oral mucosal inflammation remain unclear. (), a pathogen well-characterized in mucosal immunity and immune regulation studies, has been observed to be enriched in chronic oral inflammatory lesions and was reported to modulate T helper 17 cells (Th17)/T regulatory cells (Treg) homeostasis. Here, we developed an oral mucositis mouse model via tongue scratch and topical application to investigate its role in Th17/Treg imbalance.
The inflammatory infiltration was evaluated by macroscopic photography and HE staining. The expression of inflammatory factors in tongue tissue and peripheral blood of mice were detected by immunohistochemical staining and enzyme-linked immunosorbent assay. The number of Th17 and Treg in mice spleen lymphocytes were evaluated with flow cytometry. Differential gene expression analysis, functional enrichment analysis and immune infiltration analysis were performed using RNA-seq data from oral lichen planus (OLP).
stimulation aggravated inflammatory responses induced by scratching in lingual mucosa of mice, including increased local and systemic expression of interleukin 6 (IL6), interleukin 17 (IL17), chemokine receptor 6 (CCR6) and chemokine C-C motif ligand 20 (CCL20), increased proportions of Th17 cells and increased Th17/Treg ratio in spleen lymphocytes. Analysis of RNA-seq data from OLP revealed alterations in antimicrobial responses and inflammatory factors associated with upregulation of Th17/Treg balance.
This study supports the role of in promoting oral mucosal inflammation and provides an experimental basis for study of OLP from the perspective of microorganisms.
微生物群落失调与黏膜免疫调节异常相关，但特定细菌对口腔黏膜炎症的具体作用仍不清楚。（某病原体）在黏膜免疫和免疫调节研究中已得到充分表征，在慢性口腔炎性病变中观察到其丰度增加，且有报道称其可调节辅助性T细胞17（Th17）/调节性T细胞（Treg）的稳态。在此，我们通过舌部刮擦和局部应用建立了口腔黏膜炎小鼠模型，以研究其在Th17/Treg失衡中的作用。
通过宏观摄影和苏木精-伊红（HE）染色评估炎症浸润情况。采用免疫组织化学染色和酶联免疫吸附测定法检测小鼠舌组织和外周血中炎性因子的表达。用流式细胞术评估小鼠脾脏淋巴细胞中Th17和Treg的数量。利用口腔扁平苔藓（OLP）的RNA测序（RNA-seq）数据进行差异基因表达分析、功能富集分析和免疫浸润分析。
（某病原体）刺激加剧了小鼠舌黏膜刮擦诱导的炎症反应，包括白细胞介素6（IL6）、白细胞介素17（IL17）、趋化因子受体6（CCR6）和趋化因子C-C基序配体20（CCL20）的局部和全身表达增加，Th17细胞比例增加，脾脏淋巴细胞中Th17/Treg比值升高。对OLP的RNA-seq数据的分析揭示了与Th17/Treg平衡上调相关的抗菌反应和炎性因子的改变。
本研究支持（某病原体）在促进口腔黏膜炎症中的作用，并从微生物角度为OLP的研究提供了实验依据。
