Suppressing autophagy: a strategy by Escherichia coli O157:H7 for its survival on host epithelial cells

The primary function of autophagy is to degrade aged or impaired organelles, thus allowing cells to survive under extreme environments and rejuvenate cellular function. Besides the self-fulfillment function, autophagy also serves as a defense mechanism to invasive bacteria. Upon infection, autophagy is activated to engulf vesicles containing pathogenic bacteria for degradation. Conversely, to persist in host cells, coevolved pathogens develop sophisticated tactics to evade the trap of autophagy using various strategies. A recent publication shows that RavZ, a cysteine protease-like factor of intracellular pathogen Legionella pneumophila decreases the microtubule-associated protein 1 light chain-3B II (LC3BII) level by irreversibly blocking the conversion from LC3BI to LC3BII 1 . Likewise, pathogenicity islands 2 (SPI-2) of Salmonella Typhimurium manipulates host autophagy by actively regulating focal adhesion kinase (FAK) 2 .