My research interests lie in the field of immunotoxicology - specifically the effects of inhaled toxins and particulates on pulmonary epithelial cells and alveolar macrophages.

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Overview

Environmental Exposures:

1) Chronic Obstructive Pulmonary Disease (COPD)
 

COPD is a progressive lung disease primary caused by cigarette smoke. COPD is composed of two separate lung diseases; emphysema and chronic bronchitis. As COPD progresses patients loss their ability to breath leading to shortness of breath, disability and ultimately death. Because the prevalence of COPD is estimated to increase in the coming decades, it is imperative to identify novel therapeutic approaches to reduce the progression of COPD by targeting cellular pathways involved in COPD pathogenesis.

One protective pathway involved in COPD includes a redox sensitive transcription factor, nuclear factor-erythroid 2 p45-related factor 2 (Nrf2). Nrf2 is a member of the cap ‘n’ collar family of basic leucine zipper transcription factors that regulate the expression of many antioxidant and cytoprotective pathway genes. We hypothesize that sustained activation of Nrf2 will increase antioxidant and cytoprotective pathways to inhibit inflammation and tissue destruction generated by CS.

2) Immunomodulatory Effects of Inhaled Toxicants and Particulates
 

Inhalation of environmental or occupational toxicants can have detrimental effects on lung function, however, mounting evidence indicates that exposure to pulmonary toxins over time can alter systemic processes. Chronic exposure to silica, asbestos, road dust and other particulates leads to abnormal immunological responses such as the production of autoantibodies and possibly the development of autoimmunity.