Angela Haczku, a leading researcher on environmental causes for airway inflammation, will receive more than $900,000 from the Tobacco Related-Disease Research Program to study chronic obstructive pulmonary disease (COPD) and ozone, a toxic component of urban smog.
Haczku will use the funding to study how mouse models and patients from the UC Davis COPD Clinic respond to ozone exposure.
She and her team previously discovered that certain immune cells in lungs (group 2 innate lymphoid cells, or ILC2s) mediate the inflammatory effects of ozone inhalation. They propose that these cells could be responsible for COPD exacerbations, or episodes when lung function rapidly declines and results in the need for rescue medication and hospitalization.
“COPD is most often caused by tobacco use, however quitting after many years of smoking does little to reverse its progress,” said Haczku, professor of pulmonary, critical care and sleep medicine at UC Davis Health. “This funding helps with the efforts of my lab to determine how environmental exposures — beyond tobacco — could make patients more susceptible to exacerbations and advance the disease.”
Haczku’s new study will focus on interactions between pro-inflammatory ILC2s and surfactant protein-D (SP-D), a protective molecule in the lung, along with how those interactions change following ozone exposure and affect lung health.
“Understanding the SP-D/ILC2/inflammation axis in COPD and identifying a potential new therapeutic target for COPD are the main goals of this project,” she said.
COPD costs $50 billion in health care expenditures and is currently the third leading cause of death in the U.S., which is why understanding and developing strategies to prevent it are priorities for the Tobacco Related-Disease Research Program. The program is funded through California’s Tobacco Tax and Health Protection Act and individual contributions.
More information on UC Davis Health, including its Division of Pulmonary, Critical Care and Sleep Medicine, is at health.ucdavis.edu.