Mechanisms of lactic acid bacteria secretions as anti-Helicobacter pylori agents
Abstract
Helicobacter pylori (HP) affects 50% of the population and 1-10% of infections lead to gastric ulcers. HP utilizes virulence factors like urease activity, CagA to induce IL8 secretion from gastric cells, and flagella for motility. Mounting antibiotic resistance of HP necessitates new treatments. Lactic acid bacteria (LAB) secretions have anti-HP activity effects. Sensor kinases (SKs) sense small molecules and initiate downstream signaling cascades and the SKs HP0165 and HP0244 control the urease response and motility. They are thus potentially involved in mediating the responses to LAB secretions. We show the role of the HP SKs in the LAB supernatant context using knockout mutant studies and RNA-Seq on gastric cells infected with LAB-treated HP and work towards identifying the active molecules the SKs sense via metabolomics and quantitative proteomics. This work may lead to a novel treatment of HP as an alternative to antibiotics.