Our Research

Intestinal commensal bacteria capture components from the host diet for their own metabolic needs, but in the process produce immunoregulatory metabolites such as short-chain fatty acids (SCFAs) and secondary bile acids through modification of diet and host-derived molecules. There has been a dramatic escalation of antibiotic use worldwide to combat the emergence of antibiotic-resistant bacteria, which unintentionally target gut commensals. Disruption of a healthy microbiota may also license the outgrowth of commensals that can become pathogenic, such as the Gram-positive bacterium Clostridioides difficile. Numerous clinical and epidemiological studies suggest that the use of antibiotics increases the risk of developing autoimmune, autoinflammatory and infectious diseases, including those linked to dysregulated cell death and defective clearance of dying cells (e.g., inflammatory bowel disease (IBD), rheumatoid arthritis and diabetes). Moreover, the microbiota composition in healthy patients greatly differs from those affected with immune-related diseases, and how these differences may affect disease onset and pathology remains largely unknown. The central theme of our research program is to understand the intricate biology of host-microbe interactions, and how this shapes host immunity in health and disease. We focus on the following topics:

1) Mechanisms by which the microbiota and its byproducts regulate physiological processes, how this affects immune cell function, and how these systems are linked to protection against or susceptibility to the development of autoinflammatory, autoimmune, malignant and infectious diseases.

2) Innate immune mechanisms of host-pathogen interaction that arise as a consequence of microbiome imbalance, with a focus on host cell death and innate immune receptors.

3) Myeloid cell development and function in health and disease at the organismal level.