Researchers understand why smokers' lungs don't get better
28 July 2011
Cigarette smoke exposure fundamentally alters airway tissue in people with chronic obstructive pulmonary disease (COPD), and even while other aspects of health improve, the lung damage lasts long after a smoker quits, University of Sydney researchers have found.
COPD is the fifth leading cause of death in Australia, taking more lives than skin cancer and breast cancer combined, said the lead researcher David Krimmer of the Woolcock Institute of Medical Research at the University of Sydney.
Working with senior investigator Dr Brian Oliver, PhD candidate Mr Krimmer found smoking lays the groundwork for airway thickening, and even precipitates precancerous changes in cell proliferation that may be self-perpetuating long after cigarette smoke exposure ends.
"We have demonstrated for the first time that the extracellular matrix (ECM) produced by fibroblasts following stimulation with cigarette smoke extract is functionally different than non-exposed ECM, and that the cigarette smoke itself may prime the airways in such a way to create an environment whereby airway remodeling is encouraged," they write in an online paper, prior to publication in the American Journal of Respiratory Cell and Molecular Biology.
COPD is projected to be the third-leading cause of death worldwide by 2020, and is characterised by emphysematous destruction of the alveoli and thickening of the airway wall. The primary cause is chronic exposure to air pollution, most often cigarette smoke.
The researchers examined the response of human lung tissue from donors with and without COPD to cigarette smoke extract (CSE). They found CSE exposure led to changes in the tissue of donors with COPD over the tissue of individuals without COPD.
Similarly, they found CSE increased levels of perlecan — a protein associated with tumor growth and angiogenesis — in COPD lung tissue. These findings demonstrate cigarette smoke has the capacity to directly change the make-up of the airways. "This will change the way researchers think about the development of fibrosis in COPD," said Mr Krimmer.
"We have known for a long time that development of fibrosis is irreversible in people with COPD. Our findings suggest that cigarette smoking alters the lung composition in such a way that fibrosis becomes self-perpetuating," explained Mr Krimmer.
"Cigarette smoking is obviously bad for everyone. However, in light of our findings, cigarette smoking is likely to be especially dangerous in people with pre-existing COPD," he said.
"It is our hope that further research on how and why this occurs will result in viable therapeutic targets for reducing the detrimental airway changes underlying COPD."
|Follow University of Sydney Media on Twitter|
Interview contact: Dave Krimmer, Woolcock Institute of Medical Research, 0419 164 743, 9114 0310, firstname.lastname@example.org
Media enquiries: Kath Kenny (Mon, Wed, Thurs), 0478 303 173, 9351 1584, email@example.com
Victoria Hollick (Tues, Fri), 0401 711 361, 9351 2579, firstname.lastname@example.org