Journal of clinical periodontology · 2025
Periodontitis Induces Arterial Microbiota Shifts and Immune Dysregulation Contributing to Peripheral Vascular Inflammation.
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Zhu Xuanzhi, Cheng Shouzheng, Ge Jinting, Weng Chengxin, Fang Kun, Chen Jiali, Yang Renjie, Shi Bing, Shao Dan, Zhao Lei, Leong Kam W, Wu Yafei, Huang Hanyao
Аннотация
AIM: To explore periodontitis-induced changes in the femoral artery microbiota and their impact on the immune system, seeking to clarify the mechanisms underlying the link between periodontitis and peripheral arterial diseases (PADs).
MATERIALS AND METHODS: A ligature-induced periodontitis mouse model was used. 2bRAD sequencing for microbiome (2bRAD-M) was applied to analyse the femoral artery microbiota, and single-cell RNA sequencing (scRNA-seq) was used to characterise the arterial immune microenvironment.
RESULTS: Periodontitis significantly altered the femoral artery microbiota. There was increase in the relative abundance of anaerobic bacteria and reduction in aerobic and facultative anaerobic bacteria. Lipopolysaccharide (LPS) concentrations in both blood and the femoral artery were elevated. scRNA-seq showed an increase in fatty acid binding protein 4 (FABP4+) endothelial cells (ECs). FABP4+ ECs were more responsive to LPS, which promoted neutrophil infiltration and T-cell differentiation.
CONCLUSION: These findings identify FABP4+ ECs as key mediators in the connection between periodontitis and PADs. The study provides new insights into the systemic effects of periodontitis and offers a basis for developing preventive and therapeutic strategies for periodontitis-associated vascular diseases.
MATERIALS AND METHODS: A ligature-induced periodontitis mouse model was used. 2bRAD sequencing for microbiome (2bRAD-M) was applied to analyse the femoral artery microbiota, and single-cell RNA sequencing (scRNA-seq) was used to characterise the arterial immune microenvironment.
RESULTS: Periodontitis significantly altered the femoral artery microbiota. There was increase in the relative abundance of anaerobic bacteria and reduction in aerobic and facultative anaerobic bacteria. Lipopolysaccharide (LPS) concentrations in both blood and the femoral artery were elevated. scRNA-seq showed an increase in fatty acid binding protein 4 (FABP4+) endothelial cells (ECs). FABP4+ ECs were more responsive to LPS, which promoted neutrophil infiltration and T-cell differentiation.
CONCLUSION: These findings identify FABP4+ ECs as key mediators in the connection between periodontitis and PADs. The study provides new insights into the systemic effects of periodontitis and offers a basis for developing preventive and therapeutic strategies for periodontitis-associated vascular diseases.