Abstract
The incidence of pulmonary nontuberculous mycobacterial (NTM) infection is increasing worldwide, and its clinical outcomes with current chemotherapies are unsatisfactory. The incidence of tuberculosis (TB) is still high in Africa, and the existence of drug-resistant tuberculosis is also an important issue for treatment. To discover and develop new efficacious anti-mycobacterial treatments, it is important to understand the host-defense mechanisms against mycobacterial infection. Nuclear erythroid 2 p45-related factor-2 (NRF2) is known to be a major regulator of various antioxidant response element (ARE)-driven cytoprotective gene expressions, and its protective role has been demonstrated in infections. However, there are not many papers or reviews regarding the role of NRF2 in mycobacterial infectious disease. Therefore, this review focuses on the role of NRF2 in the pathogenesis of Mycobacterium tuberculosis and Mycobacterium avium infection.
Highlights
The incidence of pulmonary nontuberculous mycobacterial (NTM) infection is increasing worldwide [1,2], and its clinical outcomes with current chemotherapies are unsatisfactory
Shiozawa et al reported with N-acetyl cysteine (NAC) inhibited bacterial growth in both wild-type and gp91Phox−/− macrophages, that NAC-mediated protection against M. avium occurs through induction of an antibacthey suggested that the antimicrobial activity of NAC is not dependent on a fully functional terial peptide human β-defensin-2 (HBD-2) in A549 cells and murine β-defensin-3 in a host nicotinamide adenine dinucleotide phosphate (NADPH) oxidase system
reactive oxygen species (ROS) and reactive nitrogen species (RNS) are generated by phagocytic cells in response to invaded pathogens
Summary
The incidence of pulmonary nontuberculous mycobacterial (NTM) infection is increasing worldwide [1,2], and its clinical outcomes with current chemotherapies are unsatisfactory. To discover and develop new efficacious anti-mycobacterial treatments, it is important to understand the host-defense mechanisms against mycobacterial infection. The possibilities of developing new therapeutic options targeting NRF2 and oxidative stress for NTM and TB infections are discussed. The incidence and prevalence of pulmonary NTM infection have increased worldwide in recent decades [1,2]. Innovative advances in terms of pathophysiology and diagnostic and treatment methods are needed to overcome the increase in pulmonary NTM disease. It is very important to understand the pathophysiology of mycobacterial infection in order to develop new efficacious anti-mycobacterial treatments and to control the refractory diseases, such as MDR-TB and MAC diseases. The focus is on the role of NRF2 in the pathogenesis in M. tuberculosis and M. avium infections
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