Oral Pathobionts Aggravate Myocardial Infarction Through Mobilization of B2 Cells
Authors' conclusion
Oral pathobionts and proinflammatory B2 cells significantly exacerbate MI, supporting the oral-heart axis as a novel pathogenic pathway.
Study context
- Population
- Mice with ligature-induced periodontitis (PD) and myocardial infarction (MI); patients with MI with or without PD
- Comparison
- PD vs no PD in MI
- Outcome
- Effect of PD on MI severity and the bacterial and immune mechanisms involved
Methodological detailsmouse model, gnotobiotic mice, knockout mouse strains, patient cohort
- Mouse model
- Gnotobiotic mice
- Knockout mouse strains
- Patient cohort
Main finding
As reported in the abstract
- Ligature-induced PD and subgingival plaques of patients with PD exacerbated MI in mice by oral pathobionts
- Prevotella intermedia, Fusobacterium nucleatum, Selenomonas sputigena, Porphyromonas gingivalis and Bacteroides plebeius expanded in the oral cavity and ectopically accumulated in infarcted hearts through impairment of epithelial and endothelial cell barriers
- Oral pathobionts mobilized B cells, particularly B2 cells producing interleukin-6 and tumor necrosis factor-α, to aggravate MI
- Oral pathobiont-promoted B cells egress from cervical lymph nodes by a sphingosine-1-phosphate–sphingosine-1-phosphate receptor axis and infiltrate infarcted hearts by a C-X-C motif chemokine ligand 13–C-X-C motif chemokine receptor 5 axis
Original publication
Oral Pathobionts Aggravate Myocardial Infarction Through Mobilization of B2 Cells. Circulation. Published 27 August 2025. doi:10.
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