High-fat diet induces periodontitis in mice through lipopolysaccharides (LPS) receptor signaling: protective action of estrogens.

<h4>Background</h4>A fat-enriched diet favors the development of gram negative bacteria in the intestine which is linked to the occurrence of type 2 diabetes (T2D). Interestingly, some pathogenic gram negative bacteria are commonly associated with the development of periodontitis which,...

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Autores principales: Vincent Blasco-Baque, Matteo Serino, Jean-Noël Vergnes, Elodie Riant, Pascale Loubieres, Jean-François Arnal, Pierre Gourdy, Michel Sixou, Rémy Burcelin, Philippe Kemoun
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Publicado: Public Library of Science (PLoS) 2012
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spelling oai:doaj.org-article:943504b438c6422d98310751a9a4c8032021-11-18T08:10:10ZHigh-fat diet induces periodontitis in mice through lipopolysaccharides (LPS) receptor signaling: protective action of estrogens.1932-620310.1371/journal.pone.0048220https://doaj.org/article/943504b438c6422d98310751a9a4c8032012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23133617/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>A fat-enriched diet favors the development of gram negative bacteria in the intestine which is linked to the occurrence of type 2 diabetes (T2D). Interestingly, some pathogenic gram negative bacteria are commonly associated with the development of periodontitis which, like T2D, is characterized by a chronic low-grade inflammation. Moreover, estrogens have been shown to regulate glucose homeostasis via an LPS receptor dependent immune-modulation. In this study, we evaluated whether diet-induced metabolic disease would favor the development of periodontitis in mice. In addition, the regulatory role of estrogens in this process was assessed.<h4>Methods</h4>Four-week-old C57BL6/J WT and CD14 (part of the TLR-4 machinery for LPS-recognition) knock-out female mice were ovariectomised and subcutaneously implanted with pellets releasing either placebo or 17β-estradiol (E2). Mice were then fed with either a normal chow or a high-fat diet for four weeks. The development of diabetes was monitored by an intraperitoneal glucose-tolerance test and plasma insulin concentration while periodontitis was assessed by identification of pathogens, quantification of periodontal soft tissue inflammation and alveolar bone loss.<h4>Results</h4>The fat-enriched diet increased the prevalence of periodontal pathogenic microbiota like Fusobacterium nucleatum and Prevotella intermedia, gingival inflammation and alveolar bone loss. E2 treatment prevented this effect and CD14 knock-out mice resisted high-fat diet-induced periodontal defects.<h4>Conclusions/significance</h4>Our data show that mice fed with a diabetogenic diet developed defects and microflora of tooth supporting-tissues typically associated with periodontitis. Moreover, our results suggest a causal link between the activation of the LPS pathway on innate immunity by periodontal microbiota and HFD-induced periodontitis, a pathophysiological mechanism that could be targeted by estrogens.Vincent Blasco-BaqueMatteo SerinoJean-Noël VergnesElodie RiantPascale LoubieresJean-François ArnalPierre GourdyMichel SixouRémy BurcelinPhilippe KemounPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 11, p e48220 (2012)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Vincent Blasco-Baque
Matteo Serino
Jean-Noël Vergnes
Elodie Riant
Pascale Loubieres
Jean-François Arnal
Pierre Gourdy
Michel Sixou
Rémy Burcelin
Philippe Kemoun
High-fat diet induces periodontitis in mice through lipopolysaccharides (LPS) receptor signaling: protective action of estrogens.
description <h4>Background</h4>A fat-enriched diet favors the development of gram negative bacteria in the intestine which is linked to the occurrence of type 2 diabetes (T2D). Interestingly, some pathogenic gram negative bacteria are commonly associated with the development of periodontitis which, like T2D, is characterized by a chronic low-grade inflammation. Moreover, estrogens have been shown to regulate glucose homeostasis via an LPS receptor dependent immune-modulation. In this study, we evaluated whether diet-induced metabolic disease would favor the development of periodontitis in mice. In addition, the regulatory role of estrogens in this process was assessed.<h4>Methods</h4>Four-week-old C57BL6/J WT and CD14 (part of the TLR-4 machinery for LPS-recognition) knock-out female mice were ovariectomised and subcutaneously implanted with pellets releasing either placebo or 17β-estradiol (E2). Mice were then fed with either a normal chow or a high-fat diet for four weeks. The development of diabetes was monitored by an intraperitoneal glucose-tolerance test and plasma insulin concentration while periodontitis was assessed by identification of pathogens, quantification of periodontal soft tissue inflammation and alveolar bone loss.<h4>Results</h4>The fat-enriched diet increased the prevalence of periodontal pathogenic microbiota like Fusobacterium nucleatum and Prevotella intermedia, gingival inflammation and alveolar bone loss. E2 treatment prevented this effect and CD14 knock-out mice resisted high-fat diet-induced periodontal defects.<h4>Conclusions/significance</h4>Our data show that mice fed with a diabetogenic diet developed defects and microflora of tooth supporting-tissues typically associated with periodontitis. Moreover, our results suggest a causal link between the activation of the LPS pathway on innate immunity by periodontal microbiota and HFD-induced periodontitis, a pathophysiological mechanism that could be targeted by estrogens.
format article
author Vincent Blasco-Baque
Matteo Serino
Jean-Noël Vergnes
Elodie Riant
Pascale Loubieres
Jean-François Arnal
Pierre Gourdy
Michel Sixou
Rémy Burcelin
Philippe Kemoun
author_facet Vincent Blasco-Baque
Matteo Serino
Jean-Noël Vergnes
Elodie Riant
Pascale Loubieres
Jean-François Arnal
Pierre Gourdy
Michel Sixou
Rémy Burcelin
Philippe Kemoun
author_sort Vincent Blasco-Baque
title High-fat diet induces periodontitis in mice through lipopolysaccharides (LPS) receptor signaling: protective action of estrogens.
title_short High-fat diet induces periodontitis in mice through lipopolysaccharides (LPS) receptor signaling: protective action of estrogens.
title_full High-fat diet induces periodontitis in mice through lipopolysaccharides (LPS) receptor signaling: protective action of estrogens.
title_fullStr High-fat diet induces periodontitis in mice through lipopolysaccharides (LPS) receptor signaling: protective action of estrogens.
title_full_unstemmed High-fat diet induces periodontitis in mice through lipopolysaccharides (LPS) receptor signaling: protective action of estrogens.
title_sort high-fat diet induces periodontitis in mice through lipopolysaccharides (lps) receptor signaling: protective action of estrogens.
publisher Public Library of Science (PLoS)
publishDate 2012
url https://doaj.org/article/943504b438c6422d98310751a9a4c803
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