The gastric acid determines bacterial susceptibility to the stomach and inhibits infectious agents from reaching the intestine
[5]. Urease activity is crucial for H. pylori to colonize the stomach through neutralizing the acidic environment and
providing chemotactic motility [6]. However, colonization of urease-negative H. pylori and Campylobacter jejuni is reported in patients receiving acid-reducing compounds [7,8]. Moreover,predisposed decrease of acid secretion, due to therapy, disease,or age, increased bacterial population in gastric juice [9,10].Disproportional use of proton pump inhibitors is considered to promote small intestinal bacterial overgrowth, which is prevalent in patients with irritable bowel disease (IBD) [11]. Thegastrointestinal microbiota clearly contributes to development of IBD both in mouse models and patients [12].