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Helicobacter pylori infects over 3 billion people worldwide and is the primary risk factor for gastric cancer. Most individuals infected withH. pylori develop only asymptomatic gastritis; however, some develop ulcers or gastric adenocarcinoma. We demonstrate that one previously unappreciated parameter influencingH. pylori disease outcome is variation in the preinfection host microbiota. Utilizing a mouse model, we altered the microbiota by antibiotic treatment and found that these alterations resulted in significantly loweredH. pylori -triggered inflammation. Specifically, antibiotic pretreatment reduced CD4+ T-helper cells andIfn γ transcript levels in gastric tissue afterH. pylori infection. The bacterial communities in mice with a reduced response toH. pylori displayed many differences from those in untreated mice, including significantly more cluster IV and XIVaClostridium spp., bacteria known to influence inflammation via regulatory T cell populations. Our findings suggest that microbiota composition, perhapsClostridium spp., contributes to the variable disease outcome ofH. pylori infection by altering the recruitment of CD4+ T cells to the gastric compartment. Our results suggest that gastric microbiota could be used as a diagnostic tool to determine which patients are at risk for developing severe disease.

The Degree of Helicobacter pylori-Triggered Inflammation Is Manipulated by Preinfection Host Microbiota