Altered intestinal microbiota–host mitochondria crosstalk in new onset Crohn’s disease

Walid Mottawea, Cheng-Kang Chiang, Marcus Mühlbauer, Amanda E. Starr, James Butcher, Turki Abujamel, Shelley A. Deeke, Annette Brandel, Hu Zhou, Shadi Shokralla, Mehrdad Hajibabaei, Ruth Singleton, Eric I. Benchimol, Christian Jobin (), David R. Mack (), Daniel Figeys and Alain Stintzi ()
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Walid Mottawea: Microbiology and Immunology, University of Ottawa
Cheng-Kang Chiang: Microbiology and Immunology, University of Ottawa
Marcus Mühlbauer: Hepatology and Nutrition, University of Florida
Amanda E. Starr: Microbiology and Immunology, University of Ottawa
James Butcher: Microbiology and Immunology, University of Ottawa
Turki Abujamel: Microbiology and Immunology, University of Ottawa
Shelley A. Deeke: Microbiology and Immunology, University of Ottawa
Annette Brandel: Microbiology and Immunology, University of Ottawa
Hu Zhou: Ottawa Institute of Systems Biology, University of Ottawa
Shadi Shokralla: Biodiversity Institute of Ontario, University of Guelph
Mehrdad Hajibabaei: Biodiversity Institute of Ontario, University of Guelph
Ruth Singleton: Children’s Hospital of Eastern Ontario (CHEO) Inflammatory Bowel Disease Centre and CHEO Research Institute
Eric I. Benchimol: Children’s Hospital of Eastern Ontario (CHEO) Inflammatory Bowel Disease Centre and CHEO Research Institute
Christian Jobin: University of Florida
David R. Mack: Children’s Hospital of Eastern Ontario (CHEO) Inflammatory Bowel Disease Centre and CHEO Research Institute
Daniel Figeys: Microbiology and Immunology, University of Ottawa
Alain Stintzi: Microbiology and Immunology, University of Ottawa

Nature Communications, 2016, vol. 7, issue 1, 1-14

Abstract: Abstract Intestinal microbial dysbiosis is associated with Crohn’s disease (CD). However, the mechanisms leading to the chronic mucosal inflammation that characterizes this disease remain unclear. In this report, we use systems-level approaches to study the interactions between the gut microbiota and host in new-onset paediatric patients to evaluate causality and mechanisms of disease. We report an altered host proteome in CD patients indicative of impaired mitochondrial functions. In particular, mitochondrial proteins implicated in H2S detoxification are downregulated, while the relative abundance of H2S microbial producers is increased. Network correlation analysis reveals that Atopobium parvulum controls the central hub of H2S producers. A. parvulum induces pancolitis in colitis-susceptible interleukin-10-deficient mice and this phenotype requires the presence of the intestinal microbiota. Administrating the H2S scavenger bismuth mitigates A. parvulum-induced colitis in vivo. This study reveals that host–microbiota interactions are disturbed in CD and thus provides mechanistic insights into CD pathogenesis.

Date: 2016
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DOI: 10.1038/ncomms13419

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