{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,22]],"date-time":"2026-06-22T23:51:11Z","timestamp":1782172271303,"version":"3.54.5"},"reference-count":39,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2025,1,7]],"date-time":"2025-01-07T00:00:00Z","timestamp":1736208000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,1,7]],"date-time":"2025-01-07T00:00:00Z","timestamp":1736208000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Microbiol Spectr"],"published-print":{"date-parts":[[2025,1,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:sec>\n            <jats:title\/>\n            <jats:p>\n              <jats:italic>Helicobacter pylori<\/jats:italic>\n              infects roughly half the world\u2019s population, causing gastritis, peptic ulcers, and gastric cancer in a subset. These pathologies occur in response to a chronic inflammatory state, but it is not fully understood how\n              <jats:italic>H. pylori<\/jats:italic>\n              controls this process. We characterized the inflammatory response of\n              <jats:italic>H. pylori<\/jats:italic>\n              mutants that cannot produce the quorum sensing molecule autoinducer 2 (AI-2) by deleting the gene for the AI-2 synthase,\n              <jats:italic>luxS<\/jats:italic>\n              . Our work shows that\n              <jats:italic>H. pylori luxS<\/jats:italic>\n              mutants colonize the stomach normally but recruit high numbers of CD4\n              <jats:sup>+<\/jats:sup>\n              T cells to the stomach during chronic infection. This increase in the number of CD4\n              <jats:sup>+<\/jats:sup>\n              T cells correlated with elevated expression of\n              <jats:italic>CXCL9<\/jats:italic>\n              , a chemokine important for T cell recruitment. Together, our results suggest that\n              <jats:italic>H. pylori<\/jats:italic>\n              may utilize AI-2 signaling to modulate the inflammatory response during chronic infection.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>IMPORTANCE<\/jats:title>\n            <jats:p>\n              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\n              <jats:italic>Helicobacter pylori<\/jats:italic>\n              .\n              <jats:italic>H. pylori<\/jats:italic>\n              establishes chronic infections that last for decades and lead to serious disease outcomes. How AI-2 signaling and LuxS contribute to chronic\n              <jats:italic>H. pylori<\/jats:italic>\n              infection has not been studied. In this work, we analyzed how loss of\n              <jats:italic>H. pylori<\/jats:italic>\n              -created AI-2,\n              <jats:italic>via<\/jats:italic>\n              mutation of\n              <jats:italic>luxS<\/jats:italic>\n              , affects\n              <jats:italic>H. pylori<\/jats:italic>\n              chronic infection.\n              <jats:italic>luxS<\/jats:italic>\n              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\n              <jats:italic>H. pylori<\/jats:italic>\n              LuxS may play more of a role in modulating the immune response versus colonization.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1128\/spectrum.01073-24","type":"journal-article","created":{"date-parts":[[2024,12,6]],"date-time":"2024-12-06T14:00:11Z","timestamp":1733493611000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":4,"title":["<i>Helicobacter pylori luxS<\/i>\n            mutants cause hyperinflammatory responses during chronic infection"],"prefix":"10.1128","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5917-9338","authenticated-orcid":false,"given":"Christina","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Microbiology and Environmental Toxicology, University of California Santa Cruz","place":["Santa Cruz, 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