Chronic obstructive pulmonary disease (COPD), is the third leading cause of death worldwide. Emerging evidence suggests that early life exposures, specifically those during pregnancy and the first year of life, may increase future risk of COPD. A report in the journal Lancet Respiratory Medicine suggest that up to 75% of COPD cases are associated with modifiable early life exposures. Our lab is interested in using an animal model of COPD to understand whether exposure to maternal diabetes or cigarette smoke increases the negative effects of cigarette use in adulthood. Given the link between cigarette use and COPD, this will help us understand whether maternal diabetes or cigarette use are potential risk factors for COPD.

Early life exposure to cigarette smoke is perhaps the most well defined risk factor for future lung disease in children. How early life environmental exposures are communicated to the developing offspring is an interesting area of research. Often overlooked, the amniotic fluid may be an important communication medium between the maternal environment and the developing lungs. Although we have evidence that increased levels of pro-inflammatory cytokines in the amniotic fluid can promote changes in lung development and function, we do not understand what factors might contribute to changes in the amniotic inflammatory composition or how these changes might influence cell function in the lung.

MicroRNA's act like dimmer switches for genes within a cell. They can increase or decrease the abundance of a gene depending on the needs of that cell. In asthma, levels of a specific microRNA, 200b, are lower than people without asthma. Furthermore, the severity of a persons asthma is correlated with the amount of microRNA-200b they have. We do not understand why low levels of microRNA-200b are associated with asthma or why it makes asthma worse. By understanding how microRNA-200b contributes to the development of asthma, we may be able to design treatments that restore its abundance to normal levels.

Lipid mediators, also known as eicosanoids, are molecules that are important for mediating signaling between cells. In the lung, many different eicosanoids are produced that can act on the airway smooth muscle in a variety of ways. The hydroxyeicosatetraenoic acids (HETE's) are a family of eicosanoids that are abundantly produced by airway smooth muscle and other resident cells in the lung. However, we do not yet understand what role they play in regulating airway smooth muscle physiology. We will use cell culture models to understand how these lipid mediators control different aspects of airway smooth muscle function including: proliferation, differentiation, contraction, and relaxation. This research program is funded by a NSERC Discovery Grant.

Approximately 1 in every 6 Canadians have used a vaping product, with the majority of users being young adults and youths. Unfortunately, we do not fully understand the impact of vaping on lung health. This makes it difficult to make recommendations on the safety and use of vaping products in Canada. In collaboration with Dr. Kidane, Dr. Wawryko, and Dr. Halayko, we are exploring changes to the lung transcriptome in lung tissue from young adults who vape. This knowledge will allow us to potentially identify changes in lung physiology of vaping users before the onset of chronic disease. This research program is funded by a CIHR Catalyst Grant.