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Cigarette Smoke Fuels Mucus Production in People With Bronchitis
Date:2/23/2011

WEDNESDAY, Feb. 23 (HealthDay News) -- Smoking increases the production of mucus associated with chronic bronchitis, a new study shows.

U.S. researchers conducted tests on human airway tissue and on laboratory mice, and found that cigarette smoke suppresses a protein that causes the natural death of mucus-producing cells in the airways of bronchitis patients.

The study appears online ahead of print in the American Journal of Respiratory and Critical Care Medicine.

"Although it is known that chronic mucus secretion is a hallmark of chronic bronchitis, the mechanisms underlying this condition are largely unknown. This study shows that the airway cells that secrete mucus are sustained by cigarette smoke, which suppresses a cell death-inducing protein called Bik," study author Yohannes Tesfaigzi, director of the COPD Program at Lovelace Respiratory Research Institute in Albuquerque, N.M., said in a journal news release.

"Our previous studies show that following inflammatory responses, up to 30 percent of cells lining the airways undergo death and return to the original cell numbers," he continued. "This cell death is aided in part by proteins, including Bik. Disruption of this recovery process may lead to persistent elevation of mucus cell numbers and contribute to airway obstruction found in chronic lung diseases such as chronic bronchitis."

The researchers also found that restoring Bik levels in the airways of cigarette smoke-exposed mice reduced the number of mucus-producing cells.

"These studies lay the foundation to investigate therapies that may restore expression of Bik and reduce the numbers of mucus-producing cells," Tesfaigzi said. "This method may reduce excess secretion of mucus and the airway blockages in patients with chronic bronchitis."

More information

The American Lung Association has more about chronic bronchitis.

-- Robert Preidt

SOURCE: American Journal of Respiratory and Critical Care Medicine, news release, Feb. 17, 2011


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