Abstract:
OBJECTIVE:To identify a causal mechanism responsible for the enhancement of insulin resistance and hyperglycaemia following periodontitis in mice fed a fat-enriched diet. DESIGN:We set-up a unique animal model of periodontitis in C57Bl/6 female mice by infecting the periodontal tissue with specific and alive pathogens like Porphyromonas gingivalis (Pg), Fusobacterium nucleatum and Prevotella intermedia. The mice were then fed with a diabetogenic/non-obesogenic fat-enriched diet for up to 3 months. Alveolar bone loss, periodontal microbiota dysbiosis and features of glucose metabolism were quantified. Eventually, adoptive transfer of cervical (regional) and systemic immune cells was performed to demonstrate the causal role of the cervical immune system. RESULTS:Periodontitis induced a periodontal microbiota dysbiosis without mainly affecting gut microbiota. The disease concomitantly impacted on the regional and systemic immune response impairing glucose metabolism. The transfer of cervical lymph-node cells from infected mice to naive recipients guarded against periodontitis-aggravated metabolic disease. A treatment with inactivated Pg prior to the periodontal infection induced specific antibodies against Pg and protected the mouse from periodontitis-induced dysmetabolism. Finally, a 1-month subcutaneous chronic infusion of low rates of lipopolysaccharides from Pg mimicked the impact of periodontitis on immune and metabolic parameters. CONCLUSIONS:We identified that insulin resistance in the high-fat fed mouse is enhanced by pathogen-induced periodontitis. This is caused by an adaptive immune response specifically directed against pathogens and associated with a periodontal dysbiosis.
journal_name
Gutjournal_title
Gutauthors
Blasco-Baque V,Garidou L,Pomié C,Escoula Q,Loubieres P,Le Gall-David S,Lemaitre M,Nicolas S,Klopp P,Waget A,Azalbert V,Colom A,Bonnaure-Mallet M,Kemoun P,Serino M,Burcelin Rdoi
10.1136/gutjnl-2015-309897subject
Has Abstractpub_date
2017-05-01 00:00:00pages
872-885issue
5eissn
0017-5749issn
1468-3288pii
gutjnl-2015-309897journal_volume
66pub_type
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