{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T03:05:52Z","timestamp":1789095952751,"version":"build-2803163510"},"reference-count":37,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2025,4,9]],"date-time":"2025-04-09T00:00:00Z","timestamp":1744156800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,4,9]],"date-time":"2025-04-09T00:00:00Z","timestamp":1744156800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["No. 92369115, 82422048"],"award-info":[{"award-number":["No. 92369115, 82422048"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Natural Science Foundation of Chongqing, China\uff1bChongqing Talents: Exceptional Young Talents Project","award":["No. CSTB2023NSCQMSX0402\uff1bNo. cstc2021ycjh-bgzxm0099"],"award-info":[{"award-number":["No. CSTB2023NSCQMSX0402\uff1bNo. cstc2021ycjh-bgzxm0099"]}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mBio"],"published-print":{"date-parts":[[2025,4,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:sec>\n            <jats:title\/>\n            <jats:p>\n              <jats:italic>Listeria monocytogenes,<\/jats:italic>\n              a foodborne pathogen, has the ability to invade intestinal mucosal cells, undergo intracellular proliferation, activate host immune responses, and induce diseases such as colitis. We have demonstrated that sentrin-specific protease 1 (SENP1) functions as a protective gene in the host, suppressing the inflammatory response triggered by\n              <jats:italic>Listeria monocytogenes<\/jats:italic>\n              . The host\u2019s SENP1-SIRT3 axis plays a critical role in regulating inflammation during\n              <jats:italic>Listeria monocytogenes<\/jats:italic>\n              infection. Our findings reveal that overexpression of SENP1, particularly under\n              <jats:italic>Listeria monocytogenes<\/jats:italic>\n              infection conditions (MOI = 20), effectively suppresses inflammation through modulation of glycolysis. Mechanistically, during\n              <jats:italic>Listeria monocytogenes<\/jats:italic>\n              infection, SENP1 accumulates in the mitochondria, facilitating the de-SUMOylation and activation of sirtuin 3 (SIRT3). Activated SIRT3 then regulates the deacetylation of pyruvate kinase M2 (PKM2), leading to a decrease in glycolytic intermediates, downregulation of glycolysis-related gene expression, and suppression of inflammation. Taken together, our study provides a deeper understanding of the mechanistic role of the SENP1-SIRT3 axis in the regulation of inflammation, offering novel insights, and strategies for the treatment and prevention of inflammatory diseases.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>IMPORTANCE<\/jats:title>\n            <jats:p>\n              Sentrin-specific protease 1 (SENP1)-sirtuin 3 (SIRT3) has never been reported in the regulation of bacteria-induced inflammation. Our study demonstrated that SENP1 acted as a protective factor against\n              <jats:italic>Listeria<\/jats:italic>\n              -induced inflammation by promoting SIRT3 activation and subsequent metabolic reprogramming. The SENP1-SIRT3 axis served not only as an essential signaling pathway for regulating mitochondrial metabolic responses to metabolic stress but also responds to bacterial invasion and plays a protective role in the organism. Our findings provide a basis for further research into targeting the SENP1-SIRT3 signaling pathway for the treatment of bacterial infections.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1128\/mbio.02524-24","type":"journal-article","created":{"date-parts":[[2025,3,12]],"date-time":"2025-03-12T13:00:38Z","timestamp":1741784438000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":4,"title":["SENP1-SIRT3 axis mediates glycolytic reprogramming to suppress inflammation during\n            <i>Listeria monocytogenes<\/i>\n            infection"],"prefix":"10.1128","volume":"16","author":[{"given":"Yan","family":"Xiong","sequence":"first","affiliation":[{"name":"School of Life Sciences, Chongqing University","place":["Chongqing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yongliang","family":"Du","sequence":"additional","affiliation":[{"name":"School of Life Sciences, Chongqing 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