**1. Introduction**

Disruption of the epithelium apical-junctional complex is an initial step of the process which allows many bacteria and/or its toxins to permeate across an otherwise tight mucosa. Normally, the most likely target are claudins, a family of 27 different molecules [1], essential for the maintenance of intercellular tight junctions, that viruses and bacteria such as Hepatitis C virus or *Clostridum perfringens* enterotoxin, bind to mediate their entry in hepatocytes or in human ileum epithelial cells [2, 3]. The aim of this review is to recognize the mechanisms that *Helicobacter pylori* uses to disrupt the tight junctions and invade the gastric epithelial mucosa.
