Michael Aschner, Ph.D.
Albert Einstein College of Medicine
R01ES007331, R01ES010563, R01ES020852
NIEHS grantees have uncovered the key molecular pathway involved in chronic obstructive pulmonary disease (COPD) induced by air pollution exposure. Although cigarette smoke is the most common irritant that causes COPD, at least one-fourth of people with COPD are nonsmokers and thus could have COPD linked to air pollution.
In the new study, the researchers investigated gene expression changes in mouse models with lesions similar to those induced by air pollution and in human bronchial epithelial cells after exposure to diesel exhaust particles. They found that diesel exhaust particles, a major source of particulate matter (PM) air pollution, reduced genes expression for mitochondrial complexes I and V and induced COPD-like symptoms in the mice. Treatment with taurine and 3-methyladenine (3-MA) completely restored mitochondrial gene expression levels and protected both the cells and animals from PM-induced COPD. This potential therapeutic intervention likely helped reduce harmful effects of inflammation including mitochondrial oxidative stress and intracellular degradation.
The researchers also identified 1-nitropyrene as a major toxic component of diesel exhaust particles involved in PM-induced COPD. In addition, they observed that, compared to people with normal lung function, COPD patients were more susceptible to PM because of an increased inflammatory response.
Citation: Li X, Yang H, Sun H, Lu R, Zhang C, Gao N, Meng Q, Wu S, Wang S, Aschner M, Wu J, Tang B, Gu A, Kay SA, Chen R. 2017. Taurine ameliorates particulate matter-induced emphysema by switching on mitochondrial NADH dehydrogenase genes. Proc Natl Acad Sci U S A 114(45):E9655-E9664.