Interleukin-13 contributes to the occurrence of oral submucosal fibrosis

被引:6
作者
Wang, Liping
Tang, Zhangui
Huang, Junhui
机构
[1] Cent South Univ, Hunan Key Lab Oral Hlth Res, Changsha, Peoples R China
[2] Cent South Univ, Hunan 3D Printing Engn Res Ctr Oral Care, Changsha, Peoples R China
[3] Cent South Univ, Academician Workstn Oral Maxilofacial & Regenerat, Changsha, Peoples R China
[4] Cent South Univ, Hunan Clin Res Ctr Oral Major Dis & Oral Hlth, Changsha, Peoples R China
[5] Cent South Univ, Xiangya Stomatol Hosp, Changsha, Peoples R China
[6] Cent South Univ, Xiangya Sch Stomatol, Changsha, Peoples R China
基金
中国国家自然科学基金;
关键词
arecoline; IL-13; M2-macrophages; oral submucous fibrosis; polarization; BETEL-QUID; MACROPHAGES; CANCER;
D O I
10.1111/jcmm.17761
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Oral submucous fibrosis (OSF) is a chronic progressive fibrosis disease that affects in oral mucosal tissues. Interleukin (IL)-13 has been implicated in the development of fibrosis in multiple organs. Indeed, it contributes to diseases such as pulmonary fibrosis, liver cirrhosis among others. Currently, its expression in OSF and the specific mechanisms are not well understood. The aim of this study was to investigate the role of IL-13 in OSF and further explore whether IL-13 regulates-polarization of M2-macrophages in OSF. Initially, in the tissues of patients with OSF, we observed a high expression of M2-macrophages and IL-13 protein. Additionally, we found a correlation between the expression of IL-13 and the stage of OSF. Arecoline inhibited the proliferation of fibroblasts (FBs) and promoted IL-13 production in vitro. Furthermore, our observations revealed that M2-macrophages increased upon co-culturing M0-macrophages with supernatants containing the IL-13 cytokine. In conclusion, our study demonstrated that arecoline stimulates FBs leading to increased secretion of IL-13, which in turn IL-13 leads to polarization of M2-macrophages and promotes the occurrence of OSF. This suggests that IL-13 may be a potential therapeutic target of OSF.
引用
收藏
页码:1797 / 1805
页数:9
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