Helicobacter pylori: molecular basis for colonization and survival in gastric environment and resistance to antibiotics. A short review

Helicobacter pylori is a human-specific pathogen with a strict tropism for the gastric mucosa. This bacterium infects around half of the world population and is the main responsible for gastritis, peptic ulcer and, in some cases, for the pathogenesis of gastric cancer. Nevertheless, disease development in infected subjects depends not only on the bacterium, but also on the host genetic predisposition and on environmental factors. The fascinating question of how the bacterium can survive in the gastric environment has stimulated research in this field. It is now clear that H. pylori is able to colonize and adhere to the gastric epithelium through several mechanisms, including the breakdown of urea with production of the cell-toxic ammonia. The resulting raise in pH neutralizes acidity of the stomach, thereby allowing the bacterium to safely cross the mucus layer to the epithelial surface. Current challenges regard understanding the mechanisms of antibiotic resistance and how to overcome it. Lately, an increasing H. pylori resistance rate to antibiotics has been reported and several molecular bases for this phenomenon described. In this review, we highlight the current knowledge on mechanisms supporting H. pylori resistance to gastric environment and to therapy.