Journal of clinical periodontology · 2026
Porphyromonas gingivalis Drives Trained Immunity via the Glycolysis-SIRT1 Axis to Aggravate Colitis.
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Lu Bin, Que Hanxin, Chen Tianhao, Ye Pengcheng, Wu Mengting, Yu Li, Shou Fangchun, Luo Chengxiang, Bao Junjie, Jiang Chenyue, Zheng Cheng, Wang Yi, Deng Hui
Аннотация
AIM: To investigate whether Porphyromonas gingivalis aggravates colitis through trained immunity, and to elucidate the underlying metabolic and epigenetic mechanisms.
MATERIALS AND METHODS: In vivo, bone marrow from P. gingivalis-infected mice was transplanted into recipient mice, followed by induction of colitis. In vitro, macrophages trained with P. gingivalis were subjected to lipopolysaccharide (LPS) re-stimulation to assess inflammatory cytokine production. Histone acetylation and untargeted metabolomic analysis were examined in P. gingivalis-infected macrophages.
RESULTS: Recipient mice transplanted with bone marrow from P. gingivalis-infected donors developed more severe colitis. Moreover, macrophages trained with P. gingivalis showed an enhanced inflammatory response upon LPS re-stimulation. Mechanistically, histone H3 lysine 27 acetylation (H3K27ac) was markedly increased following P. gingivalis infection and remained elevated after its removal. Furthermore, P. gingivalis drives a metabolic shift towards glycolysis, which reduces nicotinamide adenine dinucleotide (NAD+) levels and sirtuin 1 (SIRT1) activity, thereby attenuating SIRT1-mediated deacetylation of H3K27ac. Inhibiting glycolysis or activating SIRT1 reversed P. gingivalis-induced trained immunity and alleviated the aggravated colitis phenotype.
CONCLUSIONS: P. gingivalis induces trained immunity via the glycolysis-SIRT1 axis and aggravates colitis. These findings provide a novel explanation for the persistent risk of colitis associated with periodontitis.
MATERIALS AND METHODS: In vivo, bone marrow from P. gingivalis-infected mice was transplanted into recipient mice, followed by induction of colitis. In vitro, macrophages trained with P. gingivalis were subjected to lipopolysaccharide (LPS) re-stimulation to assess inflammatory cytokine production. Histone acetylation and untargeted metabolomic analysis were examined in P. gingivalis-infected macrophages.
RESULTS: Recipient mice transplanted with bone marrow from P. gingivalis-infected donors developed more severe colitis. Moreover, macrophages trained with P. gingivalis showed an enhanced inflammatory response upon LPS re-stimulation. Mechanistically, histone H3 lysine 27 acetylation (H3K27ac) was markedly increased following P. gingivalis infection and remained elevated after its removal. Furthermore, P. gingivalis drives a metabolic shift towards glycolysis, which reduces nicotinamide adenine dinucleotide (NAD+) levels and sirtuin 1 (SIRT1) activity, thereby attenuating SIRT1-mediated deacetylation of H3K27ac. Inhibiting glycolysis or activating SIRT1 reversed P. gingivalis-induced trained immunity and alleviated the aggravated colitis phenotype.
CONCLUSIONS: P. gingivalis induces trained immunity via the glycolysis-SIRT1 axis and aggravates colitis. These findings provide a novel explanation for the persistent risk of colitis associated with periodontitis.