Oral Pathobionts Aggravate Myocardial Infarction Through Mobilization of B2 Cells.

Summary

Ligature-induced periodontitis and human subgingival plaque transfer worsened MI in mice via ectopic cardiac accumulation of oral pathobionts and mobilization of reactive B2 cells. Genetic and gnotobiotic experiments identified a B cell–dependent, cytokine-modulated mechanism linking the oral microbiome to myocardial injury.

Key Findings

• Ligature-induced periodontitis and transfer of human subgingival plaques exacerbated MI in mice.
• Oral pathobionts ectopically accumulated in infarcted myocardium (sequencing and FISH evidence).
• Reactive B2 cells specific to oral pathobionts mediated MI worsening; effects modulated by cytokine pathways (e.g., IL-6, TNF-α) and chemokine signaling.
• Gnotobiotic and knockout models (Ighm, Rag1, CXCL13, S1pr) delineated a B cell–dependent mechanism.

Clinical Implications

Aggressive periodontal care and strategies to modulate oral pathobionts or B cell responses may reduce MI injury. Risk stratification could incorporate periodontal status and microbiome signatures.

Limitations

• Predominantly murine models; human interventional validation is lacking.
• Specificity of implicated pathobionts and generalizability across diverse oral microbiomes need clarification.

Future Directions

Identify and prioritize culprit oral pathobionts for targeted suppression; test periodontal and immunomodulatory interventions (e.g., B cell–directed) in MI outcomes; develop microbiome-based risk tools.