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Asthma is a disease in which inflammation of hyper-responsive airways and excessive mucus production combine to make breathing extremely difficult, and airflow can become so restricted as to be fatal. The condition is on the increase worldwide.
On a molecular level, asthma is caused by chemicals called cytokines that are produced by Th-2 lymphocyte cells of the immune system. Of these cytokines, interleukin-13 (IL-13) plays a powerful role in the triggering the symptoms of asthma. Now (Nature Medicine), scientists at the University of California, San Francisco have identified the key cells that mediate the effects of IL-13 which give rise to the characteristics of asthma. Another molecule that plays a key role in the IL-13-asthma pathway is STAT-6 (signal transducers and activators of transcription 6). STAT-6 is a transcription factor, and as such enables the production of RNA from DNA. David Erle and colleagues created transgenic mice that contained STAT-6 only in cells of the lung lining or epithelium. They found that IL-13 did not cause hyper responsiveness of airways in mice lacking STAT-6, and furthermore, only when STAT-6 was present in the epithelial cells of the lung, did mice show IL-13-hyper-responsiveness and mucus production. Thus, Erle’s team has identified the cell type and the cytokine that are key to asthma. They write, “The airway epithelium and its cell-surface IL-13 receptors are readily accessible to inhaled drugs…blocking these receptors… could provide one strategy to improve the specificity of asthma treatment.” Author contact:
Dr David Erle
Department of Medicine
Lung Biology Center
University of California
San Francisco, CA, USA
Tel: +1 415 206 5905
E-mail: erle@itsa.ucsf.edu Article available online. (C) Nature Medicine press release.
Message posted by: Trevor M. D'Souza
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