This study investigates the role of Interleukin 17(IL-17)in exacerbating periapical lesions caused by Porphyromonas gingivalis(Pg)lipopolysaccharides(LPS)in the context of metabolic disease and its potential impact on...This study investigates the role of Interleukin 17(IL-17)in exacerbating periapical lesions caused by Porphyromonas gingivalis(Pg)lipopolysaccharides(LPS)in the context of metabolic disease and its potential impact on glucose tolerance.Researchers developed a unique mouse model where mice were monocolonized with Pg to induce periapical lesions.After 1 month,they were fed a highfat diet(HFD)for 2 months to simulate metabolic disease and oral microbiota dysbiosis.To explore the role of LPS from Pg,wildtype(WT)mice were challenged with purified LPS from Porphyromonas gingivalis,as well as with LPS-depleted and non-depleted Pg bacteria;IL-17 knockout(KO)mice were also included to assess the role of IL-17 signaling.The impact on bone lysis,periapical injury,glucose intolerance,and immune response was assessed.Results showed that in WT mice,the presence of LPS significantly worsened bone lysis,Th17 cell recruitment,and periapical injury.IL-17 KO mice exhibited reduced bone loss,glucose intolerance,and immune cell infiltration.Additionally,inflammatory markers in adipose tissue were lower in IL-17 KO mice,despite increased dysbiosis.The findings suggest that IL-17 plays a critical role in amplifying Pg-induced periapical lesions and systemic metabolic disturbances.Targeting IL-17 recruitment could offer a novel approach to improving glycemic control and reducing type 2 diabetes(T2D)risk in individuals with periapical disease.展开更多
基金supported by the Paul Calas Award from the French Society of Endodontics(SFE)。
文摘This study investigates the role of Interleukin 17(IL-17)in exacerbating periapical lesions caused by Porphyromonas gingivalis(Pg)lipopolysaccharides(LPS)in the context of metabolic disease and its potential impact on glucose tolerance.Researchers developed a unique mouse model where mice were monocolonized with Pg to induce periapical lesions.After 1 month,they were fed a highfat diet(HFD)for 2 months to simulate metabolic disease and oral microbiota dysbiosis.To explore the role of LPS from Pg,wildtype(WT)mice were challenged with purified LPS from Porphyromonas gingivalis,as well as with LPS-depleted and non-depleted Pg bacteria;IL-17 knockout(KO)mice were also included to assess the role of IL-17 signaling.The impact on bone lysis,periapical injury,glucose intolerance,and immune response was assessed.Results showed that in WT mice,the presence of LPS significantly worsened bone lysis,Th17 cell recruitment,and periapical injury.IL-17 KO mice exhibited reduced bone loss,glucose intolerance,and immune cell infiltration.Additionally,inflammatory markers in adipose tissue were lower in IL-17 KO mice,despite increased dysbiosis.The findings suggest that IL-17 plays a critical role in amplifying Pg-induced periapical lesions and systemic metabolic disturbances.Targeting IL-17 recruitment could offer a novel approach to improving glycemic control and reducing type 2 diabetes(T2D)risk in individuals with periapical disease.
