Too Much of a Good Thing

Davis researchers find insight into the cause of COPD

 Article by Hudson Lofchie
Photo Courtesy
Published in The California Aggie (theaggie.org) on April 11, 2012
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While it has long been known that smoking can cause serious health problems, researchers at UC Davis have been conducting research that shows how smoking causes an immune response that compounds the harm of smoking. The focus of the research has been on chronic obstructive pulmonary disease, or COPD, and the surprising discovery is that COPD arises from excess immune cells entering the lung tissue.

“Eighty percent of people with COPD are smokers,” said Kent Pinkerton, a professor in the UC Davis School of Medicine and director of the Center for Health and the Environment. “COPD is related to both asthma and emphysema. It is a serious disease that makes it hard to breathe and causes tissue damage in the lungs.”
COPD is considered a very deadly disease, killing nearly three million people every year just in the United States. In patients with COPD, tissue inflammation in the lungs skews the delicate balance of cells that line the airways. This leads to increased vulnerability to infection and a reduced ability to remove harmful inhaled particles.
Exposure to tobacco smoke, or any other kind of smoke, stimulates the release of a specific type of white blood cell called a neutrophil. The neutrophils move out of the bronchial blood vessels (the blood vessels surrounding the lungs) and accumulate in the lung tissue. In normal circumstances, neutrophils are an important aid in tissue repair, but when they are present in excess, as they are in COPD, they release enzymes that kill healthy cells and accelerate the damage they are meant to repair.
Since the body’s natural repair mechanisms have gone haywire, researchers are looking for ways to supplement the body’s natural defense and repair mechanisms to aid in recovery. They also hope to use this understanding to find a treatment.
“Understanding how a disease begins is an important step to develop new therapies, and knowing the mechanism and location of [neutrophil] recruitment … will allow us to more rapidly screen drugs and determine how they work,” said Benjamin Davis, a researcher at the Center for Health and the Environment at UC Davis and the lead author of the study. “The ultimate test comes when a treatment is transitioned from the lab to COPD patients.”
In order to discern the mechanism underlying COPD, Davis and his colleagues used an animal model of COPD to illustrate the effect of what approximately 10 years of one-pack-per-day smoking has on the immune response inside the lungs. In the animal model, which was accurately reproduced many times, the bronchial airways were completely scarred. The scarring accelerated inflammation and altered cellular makeups, leading to greatly reduced air flow and lung function.
“We used methods that could properly account for these important features of the study data while also being simple for readers to understand,” said Daniel Tancredi, an assistant professor at the UC Davis School of Medicine Center for Healthcare Policy and Research, and a statistician on the research project.
Given the large amount of research coming out on the effects of smoking, Tancredi said that it is more important than ever for researchers to make their research accessible to, and understandable by, the general public.
“We are trying to save lives,” Davis said.
According to the World Health Organization, COPD is the fourth largest cause of death in the world, accounting for about six percent of deaths worldwide.
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