Am j resp cell mol: how vitamin A helps the pulmonary immune system fight tuberculosis

June 18, 2018 / BIOON / - vitamin A deficiency can accurately predict the risk of tuberculosis (TB) in people exposed to Mycobacterium tuberculosis (MTB) Due to the increasing number of antibiotic resistant TB patients in the world, it is urgent to develop new adjuvant therapy targeting host cells to treat TB Alveolar macrophages (AM), the nest of MTB, metabolize vitamin A to all trans retinoic acid (ATRA), which can affect the host immune response To this end, the researchers tried to explore the mechanism of ATRA in primary mouse and human macrophages on host immune response to intracellular bacterial infection The researchers found that ATRA reduced the number of bacteria in human macrophages infected with MTB and Bordetella pertussis by promoting autophagy, but had no effect on BCG Autophagy can sense the production of double stranded DNA in cytoplasm through sting / tbk1 / IRF3 signal axis, but BCG is known to avoid DNA receptors in cytoplasm ATRA can promote the co localization of MTB, autophagy bodies and acid lysosomes, but it can not promote the co localization of BCG, and tbk1 can eliminate this promoting effect all the time These data suggest that ATRA enhances macrophage autophagy on intracellular bacteria that stimulate DNA receptors in the cytoplasm, but has no effect on those that do not This finding that BCG can avoid the positive impact of ATRA will have an impact on vaccine design and global health and nutrition supplement strategies The ability of ATRA to promote autophagy and assist in the clearance of MTB and B pertussis suggests that ATRA may be a potential adjuvant therapy targeting host cells Reference: Michelle m Coleman et al, all trans repetitive acid segments autophagy during internal bacterial infection, American Journal of respiratory cell and Molecular Biology (2018) Doi: 10.1165/rcmb.2017-0382oc