COMPOUND EASES LUNG INFLAMMATION CAUSED BY SMOKING
University of California, Davis
February 1, 2005
A compound that interrupts the chemical chain reaction that causes tobacco smoke to inflame the lungs has been identified in laboratory studies with rats by researchers at the University of California, Davis.
The research team, headed by respiratory biologist Kent Pinkerton and entomologist Bruce Hammock, hopes that the compound will have a similar effect in humans and lead to therapies for treating inflammation in the lungs. Their findings are published online in this week's issue of the Proceedings of the National Academy of Sciences.
Cigarette smoking is associated with a number of diseases, ranging from bronchitis to emphysema, collectively known as chronic obstructive pulmonary disease, or COPD. More than 20 million people in the United States suffer from COPD, which is the fourth leading cause of death in the U.S. Researchers suspect that, in some cases, COPD can be traced back to tobacco smoke setting off the inflammation of the lungs and airways. The inflammation process injures cells and causes an increase in mucous cells and mucus secretion. It also sometimes results in cancerous cell growth. These processes are being studied by the Pinkerton group.
The researchers were interested in a group of enzymes called sEH (soluble epoxide hydrolases), which are concentrated in the smooth muscle of the veins and arteries that carry blood between the heart and lungs. The sEH diminishes the anti-inflammatory activity of compounds called EETs (epoxyeicosatrienoic acids). Hoping to block sEH from interfering with the anti-inflammatory activity of EETs, the researchers injected rats with a compound that inhibits sEH. These rats, which are genetically predisposed to high blood pressure, provide a model for studying the inflammation process.
Each day of the three-day study, the rats were injected with the sEH inhibitor before being exposed to tobacco smoke for six hours. Some of the rats also received tiny implants that carried the anti-inflammatory EETs.
After three days of exposing the rats to tobacco smoke, the researchers found that those rats that had received injections of the sEH inhibitor experienced significantly less inflammation than did those in the control group. In addition, the rats that had been given the EETs implants experienced even less inflammation.
Because the rat form of sEH is 90 percent the same as its counterpart enzyme in humans, the researchers hope that an sEH inhibitor might also decrease smoke-caused inflammation and related disease in human lungs.
This study was supported by grants from the National Institute of Environmental Health Sciences and the University of California Systemwide Biotechnology Research and Education Program.
* Kent Pinkerton, Center for Health and the Environment, (530) 752-8334, firstname.lastname@example.org
* Pat Bailey, UC Davis News Service, (530) 752-9843, email@example.com