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.

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.

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.