<i>Helicobacter pylori luxS</i> mutants cause hyperinflammatory responses during chronic infection

Many bacteria signal to each other using quorum sensing signals. One type of signal is called autoinducer 2 (AI-2), which is produced and sensed by the LuxS enzyme found in many bacteria, including the gastric pathogen <i>Helicobacter pylori</i>. <i>H. pylori</i> establishes chronic infections that last for decades and lead to serious disease outcomes. How AI-2 signaling and LuxS contribute to chronic <i>H. pylori</i> infection has not been studied. In this work, we analyzed how loss of <i>H. pylori</i>-created AI-2, <i>via</i> mutation of <i>luxS</i>, affects <i>H. pylori</i> chronic infection. <i>luxS</i> mutants did not have significant colonization defects, similar to their reported phenotype during early infection, but they did have high stomach levels of effector and regulatory T cells and T-cell-recruiting chemokines. These results suggest that <i>H. pylori</i> LuxS may play more of a role in modulating the immune response versus colonization.