Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMCOpen access

Adipose tissue inflammation mediated by CCL19 overexpression exacerbates experimental periodontitis via elevated circulating saturated fatty acids and osteopontin in Western-diet-fed mice

Ryo N., Shinjo T., Shida M., Sato K., Otsuka H., Dilimulati G.

Animal Study, published in Front Immunol (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Front Immunol (2026)
Reported sample size
—
Source database
Europe PMC
PMID
42148137
PMCID
PMC13176198
DOI
10.3389/fimmu.2026.1787572

Abstract (original English)

Introduction Individuals with obesity may be at a higher risk of developing severe periodontitis. We previously reported that C-C motif ligand 19 (CCL19) plays a pivotal role in adipose inflammation in obesity and that adipocyte-specific Ccl19 knock-in (CCL19-KI) mice exhibited greater inflammatory cell infiltration in visceral fat, increased weight gain, and abnormal glucose metabolism than wild-type (WT) mice under a 40% high-fat diet (HFD). In this study, we examined the susceptibility of mice fed diets with different fat contents to the severity of experimental periodontitis. Methods Six-week-old male WT and CCL19-KI mice were fed either a normal diet (ND), 40% HFD, or 60% HFD for 8 weeks, after which ligature-induced periodontitis (LIP) was established. Two weeks after ligation, alveolar bone resorption, gingival inflammatory and osteoclastogenic gene expression, and serum free fatty acid (FFA) levels were compared among the groups. Additionally, RNA-sequencing (RNA-seq) was performed on epididymal white adipose tissue (eWAT) of each ligatured mouse to explore potential factors mediating periodontitis aggravation. Furthermore, in vitro studies using macrophages were conducted to investigate a possible mechanism in the progression of periodontitis. Results Alveolar bone resorption, gingival inflammatory and osteoclastogenic gene expression, and serum FFA levels were signifi

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
Adipose TissueAnimalsMice, Inbred C57BLMicePeriodontitisObesityDisease Models, AnimalInflammationFatty AcidsMale

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