A form of a gene called MSR-1 seems to influence whether a smoker will develop lung problems such as emphysema and chronic bronchitis, new research shows.
These lung conditions are classified under the umbrella term chronic obstructive pulmonary disease (COPD), which denotes problems moving air into and out of the lungs. “Clearly, the key risk factor for COPD is smoking,” Dr. Jill Ohar, from Wake Forest University Baptist Medical Center in Winston-Salem, North Carolina, told Reuters Health.
But only about 15 to 20 percent of smokers develop COPD, so presumably genetic factors must influence the risk, she explained.
Ohar said her team decided to look at the MSR-1 gene after they realized that it was involved in a number of activities that could influence the development of COPD.
MSR-1 sits on the surface of immune cells called macrophages where it helps them engulf noxious materials, she explained. Therefore, an altered form of MSR-1 could, in theory, lead to macrophages that are less effective at ridding the body of toxins, such as cigarette smoke.
In the new study, described this week at the 100th International Conference of the American Thoracic Society in Orlando, Florida, the researchers tested for different forms of the MSR-1 gene in more then 500 adults who had smoked for at least 20 years.
“We know of 10 different (forms of) the MSR-1 gene,” Ohar said. “One of these (forms)...was predictive of COPD in this group of smokers.”
This variant was identified in 17 percent of smokers with COPD, much higher than the 6 percent rate seen in smokers without COPD. This means that smokers with this form of MSR-1 are nearly three times more likely to have COPD than smokers without this form, Ohar noted.
Although the findings shed light on why some smokers develop COPD, Ohar was quick to point out that MSR-1 is probably just one of many genes that affect susceptibility to the disease.
Ohar said that by providing a better understanding of how COPD arises, research like the current study could lead to new treatments for the disease.
Revision date: July 3, 2011
Last revised: by Amalia K. Gagarina, M.S., R.D.