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 This week we profile a recent publication in Mucosal Immunology from Dr. Bill Mohn
(back row, middle) and Allisa Cait (back row, left) at UBC’s Life Sciences Institute.

Can you provide a brief overview of your lab’s current research focus?

The Mohn lab has a broad interest in microbial ecology.  We are interested in complex microbial communities and the metabolic output of these communities in many different environments including the forest soil and the human gut. In the human gut, we are most interested in metabolites produced by the microbiome, specifically short chain fatty acids, and how those metabolites can interact with immune cells in the context of allergy and asthma.

What is the significance of the findings in this publication?

There has been a recent interest in understanding how a western lifestyle can influence inflammatory disease.  Our study has shed light on the mechanism by which the gut microbiome can influence lung inflammation and highlights specific immunological pathways that are essential in this interaction. We show that gut dysbiosis can exacerbate allergic lung inflammation through both T cell and DC-dependent mechanisms, which are inhibited by short chain fatty acids. Our work emphasizes the importance of early-life exposure to commensals and their metabolites for long-term health.

What are the next steps for this research?

We are working to better understand the role of the microbiome during infant immune development.  We aim to better understand if gut dysbiosis in early life may have consequences to the systemic regulation of the immune system, particularly as this relates to allergies and asthma. We hope to apply our work in mouse models to better understand and prevent the human disease.

We are working to better understand the role of the microbiome during infant immune development.  We aim to better understand if gut dysbiosis in early life may have consequences to the systemic regulation of the immune system, particularly as this relates to allergies and asthma. We hope to apply our work in mouse models to better understand and prevent the human disease.

Read the Publication