Thoracic Surgery Department, Capital Medical University Beijing Tiantan Hospital, No.119 South Fourth Ring West Road, Fengtai District, Beijing,100070, China.
The Eighth Medical Center, Chinese PLA General Hospital, Beijing, 100091, China.
Microb Pathog. 2021 Dec;161(Pt B):105269. doi: 10.1016/j.micpath.2021.105269. Epub 2021 Nov 3.
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.
先前有报道称，硒与结核分枝杆菌（MTB）感染之间存在关联；然而，具体的机制仍不清楚。在这项研究中，与健康对照组相比，肺结核（PTB）患者的血清中的硒水平降低；它们与这些患者的治疗结果有关。qRT-PCR 检测显示，硒可能通过促炎和自噬途径发挥作用。通过诱导经典自噬和 LC3 相关吞噬（LAP），硒供体甲基硒代半胱氨酸（MSeA）的处理阻断了 MTB 感染的巨噬细胞的 M1 极化。c-Jun 在介导 MSeA 触发的经典自噬和 LAP 过程中至关重要，从而对细胞内 MTB 显示出限制作用。一项体内研究证实，MSeA 通过增强巨噬细胞自噬相关途径发挥作用。结果表明，硒通过调节巨噬细胞中的自噬对细胞内 MTB 具有限制作用。这些发现可能为未来的 PTB 治疗提供新的方向。
