By the time the lung tries to repair damage caused from smoking, it may be too late. Researchers from Washington University in conjunction with other universities revealed that lungs severely diseased by Chronic Obstructive Pulmonary Disease (COPD) try to repair themselves by creating new alveolar walls.
The lung’s restoration attempt has surprised many.
For many years now the commonly accepted scientific notion is that the air sacs, called alveolar sacs, destroyed by tobacco smoke are permanently damaged because the adult lung is incapable of producing new sacs. Until now, COPD has been perceived as a progressive disease with irreversible effects.
Prior to the report entitled, “Evidence for attempted regional elastic fiber repair in severe emphysema,” medical experts theorized that elastic fibers in alveolar walls were produced only during fetal development and early life.
The researchers, including Jason Woods, Alexander Patterson and Richard Pierce of Washington University, studied ten lungs at end stage COPD and discovered that moderately diseased parts of these lungs increased production of a gene linked to elastin fiber proliferation in an effort to repair the destroyed walls.
Elastin fibers allow the lung to expand and contract when inhaling and exhaling.
While COPD is commonly correlated with emphysema, it also comprises chronic bronchitis.
Pierce attributes the success of the research project to the collaboration of the physics and the internal medicine departments at Washington University.
“I’d like to emphasize that our collaboration with Dr. Jason Woods in the Physics department has made it possible to conduct these studies,” he said. Pierce further explained that Woods also played a pivotal role in providing undergraduate students with opportunities to participate in the venture. Kristin Castillo, a 2006 graduate, was among the student contributors who helped decipher which genes were being expressed in the diseased lungs.
“This reshapes our way of thinking about end stage emphysema,” Castillo said. “There is a possibility that the lungs can make more elastin or try to repair themselves.”
These findings may incite concerns that tobacco companies could claim that the extent of damage caused by chronic cigarette smoke exposure may not be as severe as previously perceived. But, Pierce explained that the diseased lung does not attempt to repair itself until the end stage when “it’s too little, too late.”
“The lung affected by COPD cannot stop worsening if the person continues smoking,” Pierce added.
Researchers may now focus on why the efforts of some diseased lungs fail while other lungs do not develop emphysema at all. Also, as the American Physiological Society reported, the finding “could pave the way to develop a drug to ‘turn on’ key genes to allow the lung to grow new alveoli.”
A remarkable feature of the study was that the scientists studied whole diseased lungs of patients who had already undergone successful transplants.
Pierce marveled at this extraordinary progress of science. “Here I am studying someone’s lung while they have a new lease on life and while we’re provided a new lease on discovery.”
Although “huge” is a term Pierce likes to avoid while describing the result of any scientific study, he certainly believes that his department is at the “threshold of a new thrust in lab [activity].”
He foresees meticulous focus on genetic, environmental and other factors that affect the lungs of smokers to better understand why different lungs reacts in varying degrees to the effects of smoke exposure. The efforts will be facilitated by a grant awarded to Washington University to establish a specialized center dedicated toward researching treatment of COPD. Following the route of collective efforts of different disciplines, the proposed research will comprise radiologists, physicists, lung biologists and other researchers.
“This finding is a strong step forward in our understanding of COPD and toward finding therapeutic remedies,” said Woods.