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Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
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Oral Pathobionts Aggravate Myocardial Infarction Through Mobilization of B2 Cells.

Bo-Yan Chen1,2,3,4,5, Hong Zhu1,3,4,5,6, Yu-Lin Li3,4,5

  • 1Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Engineering Research Center of Oral Biomaterials and Devices of Zhejiang Province, Hangzhou, China (B.-Y.C., H.Z., M.Y., Q.C., S.-Z.D.).

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Periodontitis exacerbates myocardial infarction (MI) by oral pathobionts that accumulate in the heart, activating inflammatory B2 cells. Targeting periodontitis and oral bacteria may improve MI treatment.

Keywords:
B-lymphocyte subsetsbacterialymph nodesmyocardial infarctionperiodontitis

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Area of Science:

  • Cardiovascular Research
  • Microbiology
  • Immunology

Background:

  • Myocardial infarction (MI) is a leading cause of mortality worldwide.
  • Periodontitis (PD) is linked to MI, but the direct impact and mechanisms are unclear.
  • The role of oral pathobionts in MI pathogenesis requires elucidation.

Purpose of the Study:

  • To investigate the direct impact of periodontitis on myocardial infarction.
  • To identify oral pathobionts involved in exacerbating MI.
  • To explore the mechanisms by which microbial signals regulate MI pathogenesis.

Main Methods:

  • A mouse model combining ligature-induced PD and MI was utilized.
  • Bacterial sequencing and FISH identified ectopic oral pathobionts in cardiac tissue.
  • Flow cytometry and gnotobiotic mice experiments characterized B2 cell responses.
  • Genetic knockout mouse strains and mutant bacterial strains were employed for mechanistic studies.
  • Human patients with MI and PD were recruited for clinical correlation.

Main Results:

  • Periodontitis and oral pathobionts exacerbated MI in a mouse model.
  • Specific oral pathobionts, including *Prevotella intermedia* and *Fusobacterium nucleatum*, were identified.
  • These pathobionts accumulated in infarcted hearts, impairing epithelial and endothelial barriers.
  • Oral pathobionts mobilized proinflammatory B2 cells, increasing MI severity.
  • B cell migration to the heart was mediated by S1P-S1PR and CXCL13-CXCR5 signaling pathways.

Conclusions:

  • Oral pathobionts and B2 cells significantly worsen MI, establishing a novel oral-heart axis.
  • Interventions targeting PD, oral pathobionts, or related immune mechanisms show therapeutic potential for MI.