Fig. 3.

H. pylori regulates autophagy in professional phagocytes. Unlike epithelial cells, both VacA, CagA and T4SS play an important role in H. pylori-induced autophagy. Recent studies have shown that HP0421, a cholesterol-α-glucosyltransferase (CGT), modulates autophagy and promotes bacterial survival in macrophages by clustering lipid rafts. The disrupted lipid rafts result in a lower internalization of H. pylori and interfere with autophagosome fusion with lysosomes. Another study has shown that H. pylori infection may increase the expression of major histocompatibility complex II (MHC II). However, TLR4 plays a negative role on BMDC maturation by inhibiting this process.