Fig. 8

Schematic presentation explains how Helicobacter pylori hijacks host-cell autophagy to favor the intracellular survival. H. pylori is a cholesterol auxotroph and converts cholesterol to cholesteryl 6ʹ-O-acyl-α-d-glucoside (CAG) by the enzymes of cholesteryl glycosyltransferase and the acyltransferase (CGAT). Our results support the idea that CGAT is mainly distributed in the subcellular compartment consisting of autophagosomes and late endosomes, in which the acidic environment is necessary for maximal enzyme activities. The elevated level of CAG can facilitate bacterial internalization, interfere with the autophagy flux, and cause reduced lysosomal biogenesis