Bilophila wadsworthia aggravates high fat diet induced metabolic dysfunctions in mice
Jane M. Natividad,
Bruno Lamas,
Hang Phuong Pham,
Marie-Laure Michel,
Dominique Rainteau,
Chantal Bridonneau,
Gregory da Costa,
Johan van Hylckama Vlieg,
Bruno Sovran,
Celia Chamignon,
Julien Planchais,
Mathias L. Richard,
Philippe Langella,
Patrick Veiga and
Harry Sokol ()
Additional contact information
Jane M. Natividad: Université Paris–Saclay
Bruno Lamas: Université Paris–Saclay
Hang Phuong Pham: ILTOO Pharma
Marie-Laure Michel: Université Paris–Saclay
Dominique Rainteau: APHP Laboratoire des Biomolécules (LBM), 27 rue de Chaligny
Chantal Bridonneau: Université Paris–Saclay
Gregory da Costa: Université Paris–Saclay
Johan van Hylckama Vlieg: Danone Nutricia Research
Bruno Sovran: Université Paris–Saclay
Celia Chamignon: Université Paris–Saclay
Julien Planchais: Université Paris–Saclay
Mathias L. Richard: Université Paris–Saclay
Philippe Langella: Université Paris–Saclay
Patrick Veiga: Danone Nutricia Research
Harry Sokol: Université Paris–Saclay
Nature Communications, 2018, vol. 9, issue 1, 1-15
Abstract:
Abstract Dietary lipids favor the growth of the pathobiont Bilophila wadsworthia, but the relevance of this expansion in metabolic syndrome pathogenesis is poorly understood. Here, we showed that B. wadsworthia synergizes with high fat diet (HFD) to promote higher inflammation, intestinal barrier dysfunction and bile acid dysmetabolism, leading to higher glucose dysmetabolism and hepatic steatosis. Host-microbiota transcriptomics analysis reveal pathways, particularly butanoate metabolism, which may underlie the metabolic effects mediated by B. wadsworthia. Pharmacological suppression of B. wadsworthia-associated inflammation demonstrate the bacterium’s intrinsic capacity to induce a negative impact on glycemic control and hepatic function. Administration of the probiotic Lactobacillus rhamnosus CNCM I-3690 limits B. wadsworthia-induced immune and metabolic impairment by limiting its expansion, reducing inflammation and reinforcing intestinal barrier. Our results suggest a new avenue for interventions against western diet-driven inflammatory and metabolic diseases.
Date: 2018
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-05249-7
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DOI: 10.1038/s41467-018-05249-7
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