ArticleFrontiers in immunology2026
Adipose tissue inflammation mediated by CCL19 overexpression exacerbates experimental periodontitis via elevated circulating saturated fatty acids and osteopontin in Western-diet-fed mice.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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 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, Results: Alveolar bone resorption, gingival inflammatory and osteoclastogenic gene expression, and serum FFA levels were significantly higher in ligated CCL19-KI mice than those in ligated WT mice under a 40% HFD. RNA-seq revealed that the OPN gene ( Conclusions: CCL19-modified adipose tissue inflammation may contribute to the severity of periodontitis via the upregulation of circulating saturated fatty acids and
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