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Polymicrobial Infection Induces Adipose Tissue Dysfunction via Gingival Extracellular Vesicles.

Y Liu1,2, B Cui1, P Zhang1

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

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Summary
This summary is machine-generated.

Periodontitis disrupts white adipose tissue (WAT) function. Gingival extracellular vesicles (gEVs) from infected mice impair WAT in healthy mice, revealing a novel pathway for periodontal disease effects.

Keywords:
extracellular vesiclesmicroRNAsperiodontal diseasestype 2 diabetes mellitus, gingivawhite adipose tissue

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Area of Science:

  • Oral Biology
  • Metabolic Disease
  • Cell Biology

Background:

  • Periodontitis is linked to metabolic dysregulation and insulin resistance.
  • The mechanisms connecting periodontitis to adipose tissue dysfunction require further investigation.
  • Extracellular vesicles (EVs) mediate intercellular communication and may link periodontitis to insulin resistance.

Purpose of the Study:

  • To investigate the impact of polymicrobial oral infection on white adipose tissue (WAT) function.
  • To explore the role of gingival EVs (gEVs) in mediating periodontitis-induced WAT dysfunction.

Main Methods:

  • Mice were infected orally with *Porphyromonas gingivalis* and *Fusobacterium nucleatum* for 14 weeks.
  • WAT function was assessed by measuring key signaling molecules and gene expression.
  • Gingival EVs (gEVs) were isolated, characterized, and their microRNA content analyzed via RNA sequencing.
  • In vitro and in vivo experiments were conducted to evaluate the effects of gEVs on WAT.

Main Results:

  • Prolonged oral infection induced WAT dysfunction, evidenced by reduced AKT phosphorylation, adiponectin, and leptin levels, and altered adipogenesis/lipogenesis gene expression.
  • RNA sequencing of gEVs revealed differentially expressed microRNAs involved in insulin signaling and adipose tissue function.
  • Gingival EVs (gEVs) from infected mice functionally mimicked plasma-derived EVs and induced WAT dysfunction in healthy recipient mice.

Conclusions:

  • Polymicrobial oral infection significantly impairs white adipose tissue (WAT) function.
  • Gingival EVs (gEVs) represent a novel mechanism by which periodontal infections can affect systemic metabolic health.
  • Targeting gEVs may offer therapeutic potential for managing metabolic complications associated with periodontitis.