Tuesday, 18 September 2012

New study offers hope for asthma sufferers


A new study has offered fresh hope for asthma sufferers by identifying ways to reduce the factors that lead to an asthma attack.  Researchers from the University of California, San Francisco (UCSF) believe they have found a way to help asthma sufferers by impeding the two most significant biological responses that lead to an asthma attack.
Researchers from UCSF, Johns Hopkins University and Duke University have demonstrated that a specific calcium activated chloride channel, holds valuable clues to reducing two biological processes that contribute to the severity of asthma. These channels regulate airway secretions and smooth muscle contraction, the two major factors that lead to an asthma attack.
“Maybe if we could inhibit both of these processes by blocking this one channel, then we could affect the two symptoms of asthma”, said senior author Jason Rock, PhD, assistant professor at the UCSF Department of Anatomy, who has had his study published in the Proceedings of the National Academy of Sciences.
Normally humans have few mucus producing cells but asthma sufferers have an elevated number of these cells in the lining of the tubes that lead to the lungs. Asthmatics also have an abnormal amount of smooth muscle surrounding the airway tubes. Even the slightest stimulus can cause these to contract.
“The overabundance of mucus plugging the airways combined with hyper contractility of the smooth muscle when the tubes get really small, make it difficult to move air in or out. A lot of people equate that with breathing through a straw”, Rock said.
Rock and his colleagues focused on a calcium activated chloride channel called TMEM16A. Rock continued, “We found that the level of this channel was increased in the mucus producing cells of asthmatics, compared to non asthmatics. And we also validated this in several models of asthma, including mouse models. That was step one.”
Step two consisted of a screen to identify chemicals that inhibit the activity of TMEM16A. The researchers identified three chemicals that inhibit the channel. Professor Rock explained, “We tested the ability of these chemicals to inhibit TMEM16A and other channels, and we found that they specifically block TMEM16A.
“It is great that we came across these molecules that were unknown previously, since we can now try to get into clinical trials to benefit patients.” Rock and his colleagues are in the pre-clinical phase to test the safety and effectiveness of the blockers in animal studies. If that goes well, Phase One of clinical trials can begin.

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