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ShareScienceDaily (Dec. 9, 2009) — A drug being tested to treat cancer could also help patients suffering from asthma, research has suggested.
Scientists at the University of Edinburgh found that the drug -- R-roscovitine -- helps to kill certain immune cells which can exacerbate symptoms associated with asthma.
The findings could lead to an alternative way to treat asthma in patients who are resistant to steroids, which are commonly used in asthma treatments.
Researchers studied the effect that the drug had on immune cells known as eosinophils
Eosinophils, found in the lungs and airways, help the body fight off parasitic infection. However, too many uncontrolled eosinophils can damage other cells that line the lung, contributing to inflammatory conditions such as asthma.
Researchers found that use of the drug caused the eosinophil cells to undergo a form of cell death known as apoptosis, a natural process where unwanted cells are removed from the body.
Professor Adriano Rossi, of the Centre for Inflammation Research at the University of Edinburgh who directed the study, said: "Steroids are commonly used to treat asthma but can have unwanted side-effects, while some asthma patients are also resistant to steroid treatment. It may well be that use of a drug, such as R-Roscovitine, or one that works in a similar same way, could offer an alternative to steroids, or be used in conjunction with steroid treatment for asthma patients."
The research has been published in the journal FEBS Letters.
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The above story is reprinted from materials provided by University of Edinburgh, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Rodger Duffin, Andrew E. Leitch, Tara A. Sheldrake, John M. Hallett, Colette Meyer, Sarah Fox, Ana L. Alessandri, Morag C. Martin, Hugh J. Brady, Mauro M. Teixeira, Ian Dransfield, Christopher Haslett, Adriano G. Rossi. The CDK inhibitor, R-roscovitine, promotes eosinophil apoptosis by down-regulation of Mcl-1. FEBS Letters, 2009; 583 (15): 2540 DOI: 10.1016/j.febslet.2009.07.017
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
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