Dr. Carolyn Baglole received her BSc and MSc from the University of Prince Edward Island, and her PhD from the University of Calgary. She then did postdoctoral research and subsequently joined the academic staff at the University of Rochester, before returning to Canada where she is currently an Associate Professor in the Departments of Pathology and Experimental Medicine at McGill
Research Interests: The research in her laboratory is aimed at identifying novel intracellular and molecular pathways that control the pathogenesis of chronic lung diseases associated with environmental exposures, particularly cigarette smoke. Her main focus is understanding how cigarette smoke-induced inflammation and cell death (apoptosis) are regulated. Chronic and persistent inflammation and the death of lung cells are involved in the etiology of lung diseases such as chronic obstructive pulmonary disease (COPD), which is almost always caused by cigarette smoke (>90% of cases). There is no cure for individuals afflicted with COPD and there are no effective therapies that can reduce disease progression. This is due, in part, to a lack of novel intracellular targets for the development of pharmacological therapies.
In this regard, her lab was the first to publish that the mere presence of a cellular receptor called the aryl hydrocarbon receptor (AhR) attenuates lung inflammation caused by cigarette smoke. This was a novel finding, as the normal physiological function of this receptor, which is best known for its ability to respond to synthetic toxicants, had not previously been described. Beyond its regulation of inflammation in the lung caused by cigarette smoke, they also investigate the role of the AhR in attenuating apoptosis, a feature that is characteristic of lung tissue destruction in COPD. Using genetic, molecular and biochemical approaches, together with in vitro and in vivo models of smoke exposure, her research is focused on establishing that the AhR is a novel and important regulator of apoptosis and understanding in vivo, and the role of the AhR in preventing morphological features of emphysema in the lung.