**10. Conclusions**

Modulation of polarized gastric epithelial cells tight junctions by *H. pylori* involves not only the direct action of some of the most recognized virulence factors of the bacteria that target individual TJ components by different pathways, but also the effect of some *H. pylori*-induced secondary or indirect mechanisms. It is clear that *H. pylori* has developed several mechanisms to endure in an organism and that invasion of the gastric mucosa is just the beginning of the bacteria survival and replicative process where suppression of the immune response is a key component that needs to be continuously explored. Nevertheless, the adhesion and invasion of the gastric mucosa epithelial cells through mechanism that favor the opening of the cell-to-cell tight junction is a bacterial strategy that allows persistent colonization and enhances its ability to cause damage to the host.
