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Cyclic di-AMP Rescues Porphyromonas gingivalis-Aggravated Atherosclerosis.

Q Wu1,2, Z Li1, Y Zhang1,2

  • 1State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Chengdu, P.R. China.

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Summary

Cyclic diadenylate monophosphate (c-di-AMP) alleviates periodontitis-exacerbated atherosclerosis by activating trained immunity. This immune modulation reduces inflammation and atherosclerotic plaque, offering a potential therapeutic strategy.

Keywords:
cardiovascular diseaseshost–pathogen interactionsmicrobial dysbiosisperiodontitissecond-messenger systemssystemic inflammation

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Area of Science:

  • Immunology
  • Cardiovascular Research
  • Microbiology

Background:

  • Periodontitis, caused by pathogens like *Porphyromonas gingivalis* (Pg), is linked to atherosclerotic cardiovascular diseases.
  • Cyclic diadenylate monophosphate (c-di-AMP) is known for its immune-adjuvant properties, activating STING and trained immunity.
  • The specific role of c-di-AMP in Pg-associated atherosclerosis remains unclear.

Purpose of the Study:

  • To investigate the role of c-di-AMP in mitigating atherosclerosis aggravated by *Porphyromonas gingivalis* infection.
  • To explore the underlying mechanisms involving trained immunity and microecological balance.

Main Methods:

  • Established periodontitis and atherosclerosis mouse models using ligature placement and high-fat diet in *ApoE* knockout mice.
  • Administered prophylactic c-di-AMP treatment to assess its effects on disease severity and inflammatory markers.
  • Analyzed gene expression of cytokines, matrix metalloproteinases, and adhesion molecules; evaluated changes in microbiota composition.

Main Results:

  • Mice exposed to Pg showed more severe periodontitis and atherosclerosis; c-di-AMP treatment significantly alleviated these conditions.
  • c-di-AMP reduced alveolar bone resorption, blood lipid levels, and atherosclerotic plaque accumulation.
  • Treatment with c-di-AMP limited the expression of pro-inflammatory cytokines (IL-6, IL-1β, TNF-α, IFN-β), MMPs, and adhesion molecules.

Conclusions:

  • Pg-induced atherosclerosis is exacerbated by inflammatory responses and altered microbiota composition.
  • c-di-AMP demonstrates a protective role by activating trained immunity, regulating immune response, and restoring microecological balance.
  • c-di-AMP represents a potential therapeutic agent for managing Pg-associated atherosclerosis.