Allergens, such as dust, pollen, and smoke, trigger airway inflammation, leading to an increase in mucus secretion. The mucus binds up the allergens and, in a process known as mucociliary clearance, ejects the allergens from the airway. Mucus is formed when dehydrated mucin molecules mix with free water in the airway. Mucus production is required to protect the airway, but in certain inflammatory airway diseases, too much mucus is produced, leading to difficulty in breathing. Mucus production is partially controlled by the number of water molecules in the airway. Water is attracted to the airway by ions, such as chloride, which are pumped out of the cells lining the airway through special channels.
In this issue of the Journal of Clinical Investigation, researchers led by Marcus Mall at the University of Heidelberg in Heidelberg, Germany, examined the role of a particular chloride channel, Slc26a9, in airway inflammation in mice. Mall and colleagues found that both wild type mice and mice lacking Slc26a9 had increased mucus production in response to airway inflammation; however, mice lacking the chloride channel developed airway mucus obstruction. Interestingly, a mutation in human SLC26A9 reduces expression of the chloride channel and is associated with asthma. This study suggests that chloride channels may serve as a target for treating airway diseases associated with mucus plugging such as asthma and cystic fibrosis.
“SLC26A9-mediated chloride secretion prevents mucus obstruction in airway inflammation” Marcus Mall, University of Heidelberg, Heidelberg, UNK, DEU
Journal of Clinical Investigation Sept. 4, 2012