Abstract
<p class="BodyText1"><em>Helicobacter pylori</em> (<em>H. pylori</em>) is detected on the surface of gastric epithelium and in goblet cells, predominantly in patients with chronic atrophic gastritis and incomplete intestinal metaplasia (IM). <em>H. pylori</em> infection persistence leads to the formation of gastrointestinal phenotype of IM. <em>H. pylori</em> 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 <em>MUC5AC</em> gene inhibition and <em>MUC2</em> gene induction. Thus, in metaplastic cells, programming differentiation after intestinal phenotype will develop. The role of <em>H. pylori</em> 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 (<em>e.g.</em>, <em>SHH</em>, <em>SOX2</em>, and <em>RUNX3</em>) responsible for gastric differentiation, was identified to cause the appearance of IM. </p>
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