To test their hypothesis, the researchers examined both human airway tissue samples and mouse models. Human samples were derived from autopsy tissues and from bronchial brushings taken from individuals with chronic bronchitis as well as healthy controls. Chronic bronchitis was defined as a daily cough with phlegm production for 3 consecutive months, 2 years in a row.
Mice were exposed to cigarette smoke for six hours per day, five days per week for three weeks. Following exposure, lung tissue samples were collected and examined for the presence of Bik.
The researchers determined Bik was significantly reduced in bronchial brushings of patients with chronic bronchitis compared to non-diseased controls. Examination of autopsy tissues confirmed the finding. Mice exposed to cigarette smoking also had significantly reduced Bik levels and increased numbers of mucus-producing cells.
In another arm of the study, mice exposed to cigarette smoke were subsequently exposed to filtered air for 60 days and evaluated for Bik levels to determine whether Bik remains suppressed even after cessation of cigarette smoking. They found mice exposed to cigarette smoke still exhibited significantly lower levels of Bik, even after being exposed to filtered air.
"We found that cigarette smoke suppresses Bik levels in humans and in mice models, and mucus cells increased threefold in mice exposed to cigarette smoke," he said. "Moreover, the mouse study suggests that Bik remains suppressed in former cigarette smokers that have persistent chronic bronchitis. In humans, Bik was reduced even more in former smokers who had chronic bronchitis compared to former smokers without.
"The possible therapeutic value of these findings was tested by restoring Bik levels in the airways of cigarette smoke-exposed mice or human airway epitheli
|Contact: Brian Kell|
American Thoracic Society