自噬
吞噬作用
细胞内
硒
细胞内寄生虫
结核分枝杆菌
巨噬细胞
促炎细胞因子
传出细胞增多
生物
化学
肺结核
微生物学
细胞生物学
免疫学
体外
医学
生物化学
炎症
细胞凋亡
病理
有机化学
作者
Wenhui Chen,Zhen Liu,Ying Zheng,Bo Wei,Jingdong Shi,Baowei Shao,Di Wang
标识
DOI:10.1016/j.micpath.2021.105269
摘要
The relationship between selenium and Mycobacterium tuberculosis (MTB) infection has been reported previously; however, the specific mechanism is still not clear. In this study, selenium levels decreased in the serum of patients with pulmonary tuberculosis (PTB) compared with the healthy controls; they were associated with the treatment outcome of such patients. The qRT-PCR assay revealed that selenium might function through proinflammatory and autophagy pathways. The treatment with methylseleninic acid (MSeA), a selenium donor, blocked the M1 polarization of MTB-infected macrophages through the induction of both canonical autophagy and LC3-associated phagocytosis (LAP). c-Jun is vital in mediating the MSeA-triggered canonical autophagy and LAP process, thus displaying a restricting function against intracellular MTB. An in vivo study confirmed that the activity of MSeA was shown through enhancing macrophage autophagy related pathway. The results showed that selenium had a restricting function against intracellular MTB by regulating autophagy in macrophages. The findings might provide a novel direction for PTB therapy in the future.
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