Grant: Travel Awards - Institute Community Support

Chronic Obstructive Pulmonary Disease (COPD) is a progressively worsening lung disease commonly caused by cigarette smoking. It affects 1 in 20 people in Canada and has been predicted to be the third leading cause of death by 2030. COPD is the 4th leading cause of death in North America and costs the Canadian health care system billions of dollars. Current drug treatments have been unsuccessful in slowing the progression of COPD, which prompted us to discover new drug classes from genes identified from large genome wide association studies (GWAS) to target COPD. A protein called Cholinergic Receptor Nicotinic Alpha 5 Subunit (CHRNA5) has been strongly involved in the risk for heavy smoking and nicotine dependence (ND). ND is directly related to the number of cigarettes smokes per days as well as the risk for COPD. Nicotine can activate this protein and increase the growth and movement of cells that line the airway tubes. When this happens, the tissue scarring may occur and reduce the flow of air moving through the lung, leading to difficulty in breathing. We will show if this protein is increased or decreased in the airway tissues in human lung tissues, and then test how this protein responses to cigarette smoke treatment in cells that line the airway tube. Effective treatment for COPD is currently limited, leading to high rates of hospitalization and mortality for COPD patients. By understanding the relationship between the biology of CHRNA5 and nicotine activation from cigarette smoke, we will be able to identify a unique way to target this disease process. This is fundamentally important in controlling the increased risks of smoking, morbidity and mortality in patients with COPD in Canada and worldwide.