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]. The
gastrointestinal microbiota clearly contributes to development of
IBD both in mouse models and patients