Helicobacter pylori as a crucial factor in intestinal metaplasia development of gastric mucosa

Helicobacter pylori  ( H. pylori ) is detected on the surface of gastric epithelium and in goblet cells, predominantly in patients with chronic atrophic gastritis and incomplete intestinal metaplasia (IM).  H. pylori  infection persistence leads to the formation of gastrointestinal phenotype of IM.  H. pylori  can be considered as an etiological factor of IM. It inhibits the expression of SOX2 in gastric epithelial cells, hence activating transcription factor CDX2 as a counterpart to  MUC5AC  gene inhibition and  MUC2  gene induction. Thus, in metaplastic cells, programming differentiation after intestinal phenotype will develop. The role of  H. pylori  in the origin of intestinal metaplasia of gastric mucosa was defined in this study to elucidate the probable mechanism of cell reprogramming. The activation of CDX2, with simultaneous inactivation and decreased number of genes ( e.g. ,  SHH ,  SOX2 , and  RUNX3 ) responsible for gastric differentiation, was identified to cause the appearance of IM.