Scientific goal

Inflammatory bowel diseases (IBD), including Crohn’s disease and ulcerative colitis, are immune-related disorders characterized by inappropriate gut inflammation. Their incidence has increased dramatically in Western countries in recent decades, supporting the role of environmental factors. Despite the development of new treatments, IBD are insufficiently controlled in a large proportion of patients, inducing an alteration in the quality of life and a socioeconomic burden. A better understanding of the pathogenesis and identification of new therapeutic targets are therefore urgently needed. 

In this context, the gut microbiota has been recognized as a strong actor in IBD. Classical host-microbiota interaction concepts rely on the recognition of conserved microbial motifs by innate immunity sensors or on the action of microbial molecules on a host cell receptor. Additionally, energy metabolism plays a crucial role in mounting the appropriate cellular response, and an alteration in intestinal and immune cell energy metabolism has been suggested in the pathogenesis. Emerging data, including ours, indicate that the gut microbiota may directly affect it. 

The hypothesis underlying the current project is that the altered gut microbiota in IBD contributes to the impairment of host cell energy metabolism and pathogenesis. 

The aims of the project are to (i) identify the microorganisms and microbiota-derived metabolites impacting host cell energy metabolism and the mechanisms involved, (ii) decipher the consequences of gut microbiota alterations on host cell energy metabolism in IBD, and design new microbiota-based therapeutic strategies to manipulate the host cell energy state in IBD.