Porphyromonas gingivalis-induced glucose intolerance during periapical lesions requires its LPS throught a Th17 immune response.
10.1038/s41368-025-00403-6
- Author:
Sylvie LÊ
1
;
Emma STURARO
1
;
Charlotte THOMAS
1
;
Thibault CANCEILL
1
;
Bertrand EKAMBI
2
;
Nawel FELLOUAH
2
;
Claude KNAUF
3
;
Anne ABOT
4
;
Christophe TENAILLEAU
5
;
Benjamin DUPLOYER
5
;
Pascale LOUBIERES
1
;
Alison PROSPER
1
;
Swann DIEMER
1
;
Rémy BURCELIN
6
;
Franck DIEMER
1
;
Matthieu MINTY
1
;
Vincent BLASCO-BAQUE
7
Author Information
1. Département d'Odontologie, Faculté de Santé, Université de Toulouse, Toulouse, France.
2. ABBIA GROUP, Abbia Data Sciences, Toulouse, France.
3. UMR1220 Inserm, Team Pathologies of the Gut-Brain Axis, Institut de Recherche en Santé Digestive (IRSD), Université de Toulouse, Toulouse, France.
4. Enterosys SAS, 57 rue de l'Innovation, Enterosys SAS, Labège, France.
5. CIRIMAT, Université de Toulouse 3 Paul Sabatier, INP, CNRS, Toulouse, France.
6. UMR1297 Inserm, Team InCOMM/Intestine ClinicOmics Metabolism & Microbiota, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Paul Sabatier, Toulouse, France.
7. Département d'Odontologie, Faculté de Santé, Université de Toulouse, Toulouse, France. vincent.blasco@inserm.fr.
- Publication Type:Journal Article
- MeSH:
Animals;
Porphyromonas gingivalis/immunology*;
Th17 Cells/immunology*;
Lipopolysaccharides/immunology*;
Mice;
Glucose Intolerance/microbiology*;
Interleukin-17/metabolism*;
Mice, Knockout;
Mice, Inbred C57BL;
Disease Models, Animal;
Diet, High-Fat;
Periapical Diseases/microbiology*;
Male;
Dysbiosis
- From:
International Journal of Oral Science
2025;17(1):69-69
- CountryChina
- Language:English
-
Abstract:
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 high-fat diet (HFD) for 2 months to simulate metabolic disease and oral microbiota dysbiosis. To explore the role of LPS from Pg, wild-type (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.
