The rise in the prevalence of COPD is a global health concern. Exposure to cigarette smoke is the most widely associated environmental risk factor for the development of the disease. Inhalation of the noxious substances in cigarette smoke induces chronic bronchitis and emphysema that lead to the progressive and irreversible airflow limitation characteristic of the disease. While patients can manifest mild to severe disease as defined by the degree of airflow obstruction, the signals leading to increased severity and progression remain unclear. In spite of the heterogeneity in human disease, it is apparent that aberrant inflammatory responses contribute substantially to the decline in lung function.
We study the mechanisms through which COPD develops and is maintained. In particular, we hypothesize that microbial dysbiosis in the lung itself, is a key instigator of disease and driver of disease chronicity.