(dailyRx)
“You can checkout any time you like, but you can never leave.” That is the scenario for smokers who develop COPD. New research indicates that once the damage is done to the extracellular matrix (ECM) in the lungs, it remains damaged even after a person stops smoking.

Lead researcher David Krimmer, a Ph.D.candidate at the Woolcock Institute of Medical Research, of the University of Sydney in Australia reports that the team has shown that ECM damage caused by fibroblasts from smoking remains functionally different even after a person stops smoking.

Researchers surmise the cigarette smoke primes the airways to create an environment that promotes airway remodeling.

Krimmer continues to explain that researchers were trying to determine if cigarette smoke alters ECM and if this smoke-induced ECM alters proliferation and cytokine release. Secondly, they investigated whether the release of cytokines from these fibroblasts were multiplied by additional cigarette smoke. Now, Krimmer predicts researchers will be approaching the etiology of fibrosis in COPD in a different way.

The researchers also included findings that cigarette smoke extract (CSE ) exposure caused the COPD tissue to become more inflamed than non-COPD tissue.

Krimmer believes the most exciting finding in this study was that CSE-induced ECM caused fibroblasts to multiply. Kimmer explains that scientists have known for a long time that once fibrosis in the lungs develops, it is irreversible in those with COPD.

These new findings suggest that once the composition of the lungs is altered by smoking, the alteration causes a self-perpetuation that is irreversible.

Krimmer summarizes by acknowledging that cigarette smoking is bad for everyone but appears particularly harmful for those with pre-existing COPD.

These findings illustrate how ECM perpetuates the disease progression of COPD even if the patient has quit smoking.

Krimmer invisions new research determining why once the ECM changes it takes on a life of its own irregardless of subsequently not having a smoker’s environment. Perhaps viable therapy targets will be derived from this research.

The researchers used two different groups of human lung tissue samples: One group of samples were from patients with COPD and the second group were from donors who did not have COPD. Both groups were exposed to cigarette smoke extract and researchers noted the different reaction patterns of each group.

The study appeared online and will be in the final publication in the American Thoracic Society’s American Journal of Respiratory Cell and Molecular Biology.