Maternal diabetes is a risk factor for asthma in offspring and has recently been assocaited with impaired lung function in children. The mechanism for this link is currently unknown, but maternal hyperglycemia appears to be involved. Our lab is using animal models and iPSC-smooth muscle cells explore how maternal hyperglycemia influences airway smooth muscle contractility and reactivity as it relates to asthma and lung dysfunciton. This project is funded by CIHR.

E-cigarettes are popular among youth, with one in every three Canadian youth between the ages of 15-19 reporting having used the devices at some point, and one in every five using them daily. This level of popularity surpasses even youth cigarette use in the early 2000’s, highlighting the growing concern that we may be witnessing the development of a new nicotine addicted generation. There are an estimated 16,000 e-liquid flavor combinations available on the market, but each of these combinations mixes a handful of specific chemicals together to create flavor profiles. While these chemicals are considered safe by health agencies, this tag applies to eating or drinking, not inhaling them through a device after heating. Currently, we know very little about how these molecules influence the health of the lung. This project will explore how specific flavor molecules, when heated, influence the toxin response of airway epithelial cells.

Smoke from wildfires burning across the country have caused concern about the short- and long-term health effects of breathing in this polluted air. Smoke contains small particles that can enter deep into the lung, causing damage and possibly contributing to difficulty breathing. How wildfire smoke exposure on short timescales (up to 1-hour) impacts the ability to comfortably breath is unknown. In this project, we are exploring whether woodsmoke, simlulating a wildfire, induces excessive airway narrowing after short exposures that might mimic what someone is exposed to while completing yard work during a wildfire smoke event. 

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.

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.