Figure 2.

Survival and adaptive mechanisms of Myobacterium tuberculosis in macrophages. Some M. tuberculosis can enter into the alveolar macrophages through a non-phagocytic pathway called clathrin-independent endocytosis. M. tuberculosis can then escape from phagosomes and release into the cytosol of macrophages. M. tuberculosis can induce the expression of anti-apoptosis genes (Bcl-2) into the macrophages. The absorption of H⁺, H₂O₂, O₂, NO₂, and OH also are inhibited to control the acidification of phagosome harboring M. tuberculosis. M. tuberculosis can escape from phagolysosome by producing ESAT-6 proteins, Wiskott-Aldrich syndrome protein (WASP), and CFP-10 chaperone. M. tuberculosis prevents transforming of primary endosomes in phagolysosome via the reducing of levels of proton ATPase inside the endosomes, connecting the inducible iNOS and elimination of the phosphatidylinositol 3-phosphate (PI3P). Tryptophan-aspartate containing coat (TACO) proteins, represents a component of the phagosome coat that is released earlier than phagosome fusion with or maturation into lysosomes. In macrophages containing TACO, it leads to preventing to forming phagolysosome and following that M. tuberculosis can survive within the phagosome.