Bruno Lamas awarded a Michael G. DeGroote Fellowship Award in Basic Biomedical Science

Bruno Lamas comes to the Verdu lab after a PhD from Auvergne University, France and a post-doctoral fellowship at UPMC University in Paris and MICALIS Institute at INRA. He is interested in the relationship between the products of metabolism and the host’s immune system, in the context of intestinal inflammatory disorders. Here at McMaster, supported by a Michael G. DeGroote Fellowship Award in Basic Biomedical Science, he will investigate the role of the gut microbiota metabolism on the inappropriate intestinal immune response observed in celiac disease patients. His long-term goal is to identify new mechanisms involved in the pathogenesis of celiac disease, that can lead to development of novel preventive and therapeutic strategies.

Approximately 300,000 Canadians suffer from celiac disease (CeD), one of the most common food sensitivities. CeD is triggered by ingestion of gluten-containing food, that causes destruction of the small intestinal lining leading to abdominal, skin and neurological symptoms. The HLA-DQ2 or -DQ8 gene is necessary, but insufficient alone, to develop CeD suggesting additional environmental factors are required. Large, undigested fractions of gluten are responsible for the development of a pathogenic gluten-specific T cell response and this, in conjunction with the activation of intraepithelial lymphocytes (IEL), leads to intestinal atrophy. The trigger(s) for IEL activation in CeD, however, remain unknown. During his PhD Bruno showed that changes in gut bacteria lead to altered production of molecules that signal through the aryl hydrocarbon receptor (AhR), which affects inflammation in the gut. Importantly, AhR influences IELs that are key for the development of intestinal damage in CeD. Thus, the central aim of his proposed work is to determine if gut bacteria from celiac patients activate IELs through impaired capacity to produce AhR ligands from tryptophan metabolism. Currently, a strict life-long gluten-free diet is the only efficient treatment available for CeD. This is financially and socially difficult for patients, contamination with hidden sources of gluten is frequent, and many patients do not respond favorably to dietary gluten restriction. Bruno’s work will identify new mechanisms involved in the innate immune activation pathway of CeD in hopes of elaborating novel preventive and therapeutic strategies based on identification of AhR-activating bacteria, or their metabolites.

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