Grant: Doctoral: Vanier Canada Graduate Scholarships

Over the past few decades, Westernized countries have seen an alarming increase in the prevalence of atopic diseases such as asthma. Although both genetic and environmental factors contribute to the pathogenesis of this disease, the rapidity at which the global asthma burden is increasing suggests that environmental factors are primarily responsible. Borne out of epidemiological studies showing associations between an altered early life gut microbiota and the later development of asthma, researchers are increasingly turning to the investigation of the gut microbiota and early life microbial exposure as potential drivers of/contributors to this phenomenon. It is now well established that colonization of the intestinal tract by particular microorganisms is critical to the development and function of the immune system, and that the microbiota plays a role in atopic diseases. Our working hypothesis is that the intestinal microbiota affects immune development and asthma, and that specific microbial populations play protective or harmful roles in these processes. Preliminary data from the Finlay lab indicate that both Canadian and Ecuadorian children with asthmatic and non-asthmatic phenotypes differ in the composition of their early life gut microbiota, and that these differences are different between the two regions. These data, combined with the knowledge that asthmatic phenotypes differ regionally across the globe, suggest that different members of the gut microbiota are differentially modulating various aspects of this airway disease. As part of a clinically relevant collaborative project, I wish to investigate the mechanisms through which certain gut microbes influence the etiology/progression of asthma. Using correlations between murine and human results, I intend to identify specific microbial species or products that aggravate or ameliorate asthma in mice and infants, and assess the effects of these species and/or their metabolic products on immune development.