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Periodontitis induced by Porphyromonas gingivalis drives periodontal microbiota dysbiosis and insulin resistance via an impaired adaptive immune response

Open access
Blasco-Baque, Vincent, Garidou, Lucile, Pomié, Céline, Escoula, Quentin, Loubieres, Pascale, Le Gall-David, Sandrine, Lemaitre, Mathieu, Nicolas, Simon, Klopp, Pascale, Waget, Aurélie, Azalbert, Vincent, Colom, André, Bonnaure-Mallet, Martine, Kemoun, Philippe, Serino, Matteo, Burcelin, Rémy·2017·Gut

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.

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Metadata

Authors
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, R.
Venue
Gut
Publisher
BMJ
Published
2016-02-02
Volume
66
Issue
5
Pages
872-885
ISSN
  • 0017-5749 (ISSN-L)
  • 1468-3288
OpenAlex
W2259258150
Cited by
320
References
49
FWCI
21.74
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Periodontitis induced by Porphyromonas gingivalis drives periodontal microbiota dysbiosis and insulin resistance via an impaired adaptive immune response. https://app.cochat.ai/papers/10.1136/gutjnl-2015-309897
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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, R. (2017). Periodontitis induced by Porphyromonas gingivalis drives periodontal microbiota dysbiosis and insulin resistance via an impaired adaptive immune response. Gut. https://doi.org/10.1136/gutjnl-2015-309897

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