The integral membrane protein LucA facilitates fatty acid and cholesterol uptake into Mycobacterium tuberculosis by stabilizing the Mce1 and Mce4 transporters, respectively, and Mce1 functions as a fatty acid transporter in Mycobacterium tuberculosis.
An in vivo drug screen of FDA-approved compounds in zebrafish identified host-directed therapies against mycobacterial infection, including the drug clemastine, which targets the P2RX7-inflammasome axis to enhance bacterial control.
Mycobacterium tuberculosis (Mtb), effectors secreted through SecA2 pathway cause double strand breaks (DSBs) in the host DNA, which in turn activates ATM kinase to gain survival advantages, through Akt.
The rapid killing of macrophages by Mycobacterium tuberculosis aggregates, and the subsequent proliferation of the bacteria inside the dead cell, leads to a cell death cascade and explains the coupling of necrosis and pathogen growth observed in active disease.
Quantifiable bioenergetic parameters, determined from extracellular flux analyses, are distinct between macrophages infected with Mycobacteriumtuberculosis or vaccine strain M. bovis BCG, enabling assessment of future vaccine and drug efficacy.