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In\u00a0vitro, macrophages trained with\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>P. gingivalis<\/jats:italic>\n                      <\/jats:styled-content>\n                      were subjected to lipopolysaccharide (LPS) re\u2010stimulation to assess inflammatory cytokine production. Histone acetylation and untargeted metabolomic analysis were examined in\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>P.\u00a0gingivalis<\/jats:italic>\n                      <\/jats:styled-content>\n                      \u2010infected macrophages.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Recipient mice transplanted with bone marrow from\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>P. gingivalis<\/jats:italic>\n                      <\/jats:styled-content>\n                      \u2010infected donors developed more severe colitis. Moreover, macrophages trained with\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>P. gingivalis<\/jats:italic>\n                      <\/jats:styled-content>\n                      showed an enhanced inflammatory response upon LPS re\u2010stimulation. Mechanistically, histone H3 lysine 27 acetylation (H3K27ac) was markedly increased following\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>P. gingivalis<\/jats:italic>\n                      <\/jats:styled-content>\n                      infection and remained elevated after its removal. Furthermore,\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>P. gingivalis<\/jats:italic>\n                      <\/jats:styled-content>\n                      drives a metabolic shift towards glycolysis, which reduces nicotinamide adenine dinucleotide (NAD\n                      <jats:sup>+<\/jats:sup>\n                      ) levels and sirtuin 1 (SIRT1) activity, thereby attenuating SIRT1\u2010mediated deacetylation of H3K27ac. Inhibiting glycolysis or activating SIRT1 reversed\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>P. gingivalis<\/jats:italic>\n                      <\/jats:styled-content>\n                      \u2010induced trained immunity and alleviated the aggravated colitis phenotype.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>P. gingivalis<\/jats:italic>\n                      <\/jats:styled-content>\n                      induces trained immunity via the glycolysis\u2013SIRT1 axis and aggravates colitis. These findings provide a novel explanation for the persistent risk of colitis associated with periodontitis.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jcpe.70179","type":"journal-article","created":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T01:41:02Z","timestamp":1785289262000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<scp>\n                      <i>Porphyromonas gingivalis<\/i>\n                    <\/scp>\n                    Drives Trained Immunity via the Glycolysis\u2013\n                    <scp>SIRT1<\/scp>\n                    Axis to Aggravate Colitis"],"prefix":"10.1111","author":[{"given":"Bin","family":"Lu","sequence":"first","affiliation":[{"name":"Institute of Stomatology, School and Hospital of Stomatology, Wenzhou Medical University  Wenzhou Zhejiang 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