Fig. 1.

Bacteria hijack lipid rafts to induce autophagy as part of their infectious strategy. Mycobacterium tuberculosis is capable of surviving in the phagosome after being internalized into the host cell by preventing phagosomal maturation and inhibiting autophagosome fusion with lysosome. M. tuberculosis is able to survive and replicate in the phagosome. However, cytosolic translocation of M. tuberculosis can occur when it expresses the early secretory antigenic target of M. tuberculosis (ESAT-6) secretion system (ESX-1) and type VII secretion system (TSSS). Listeria monocytogenes employs various virulence factors in its escape from autophagy. Upon escaping from the phagosome using its pore forming toxin (Listeriolysin O), L. monocytogenes expresses another virulence factor ActA to inhibit the recruitment of p62 and NDP52 to its surface. Another group of virulence factors, two phospholipases C (PlcA/B) then prevent the formation of the autophagosomal membrane. In Legionella infections, L. pneumophila escapes from the vacuole and enters the host’s cytosol via LepB using a type IV secretion system. The cytosolic L. pneumophila is subsequently recognized by the autophagic machinery but delays phagocytosis by using its effector protein RavZ. In the autophagosome L. pneumophila also delays the fusion of the autophagosome with lysosome to allow it time to develop into an acid-resistant form. This acid-resistant form of L. pneumophila can then replicate in the acidic autophagolysosome.