Cigarette Smoking Increases Mucus Production

The researchers hypothesized that the dysregulation of this protein causes a disruption of the expected recovery process, resulting in a persistent elevation of mucus cell numbers, thus contributing to the airway obstruction found in chronic lung diseases such as chronic bronchitis. To test their hypothesis, the researchers examined both human airway tissue samples--taken from individuals with chronic bronchitis as well as healthy controls--and mouse models from mice that were exposed to cigarette smoke for six hours per day, five days per week, for three weeks.

The researchers succeeded in identifying the protein Bcl-2-interacting killer (Bik) to be significantly reduced in bronchial brushings of patients with chronic epithelial cell hyperplasia. Reduced Bik levels were also detected when normal human airway epithelial cells (HAECs) were exposed to cigarette smoke, or when autopsy tissues from former smokers with and without chronic bronchitis were compared. Similarly, the mice exposed to cigarette smoke resulted in increased number of epithelial and mucous cells per mm basal lamina. The results suggest that cigarette smoke suppresses Bik levels in both humans and in mice models, resulting in a threefold increase in mucus cells in mice exposed to cigarette smoke. The results also suggest that Bik remains suppressed in former cigarette smokers that have persistent chronic bronchitis. The study was published early online on February 11, 2010, 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,” said lead author Yohannes Tesfaigzi, PhD, director of the Lovelace chronic obstructive pulmonary disease (COPD) program. "These studies lay the foundation to investigate therapies that may restore expression of Bik and reduce the numbers of mucus-producing cells.”

Bik is a protein that in humans is encoded by the BIK gene, known to interact with cellular and viral survival-promoting proteins, such as BCL2 and the Epstein-Barr virus in order to enhance programmed cell death. Because its activity is suppressed in the presence of survival-promoting proteins, this protein is suggested as a likely target for antiapoptotic proteins.

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Lovelace Respiratory Research Institute