Helicobacter pylori (H. pylori) colonizes approximately half of the world’s population and causes chronic gastritis, peptic ulcers, and gastric adenocarcinoma [1]. Eradication of this bacterium improves the symptoms of patients with peptic ulcer and gastric lymphoma of mucosa-associated lymphoid tissue [2,3]. Isolation of H. pylori
from endoscopic gastric biopsy specimens is the most reliable method for detecting H. pylori infection and essential for drug susceptibility testing [4].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 [12].