Selenium donor restricts the intracellular growth of Mycobacterium tuberculosis through the induction of c-Jun-mediated both canonical autophagy and LC3-associated phagocytosis of alveolar macrophages

Abstract

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.