Until now the biological reason why the lungs of people with conditions such as asthma and cystic fibrosis often clog up with thick mucus has been unclear.
It was thought that after airways were attacked by an allergic response or inflammation mucus cells, known as goblet cells, divided and proliferated at a very fast rate - a process known as hyperplasia.
But researchers at the Cincinnati Childrens’ Hospital have discovered that instead a type of lung cell, called Clara cells, morph into goblet cells - a process called metaplasia and they showed that the process was reversible - goblet cells can change back to Clara cells if the initial problem is dealt with. In work on mice, the researchers also identified a gene called SPDEF as key to the process of mucus production.
The researchers used a protein from egg whites to induce an allergic reaction in inflammation in the animals' lungs, and showed that SPDEF activity soared in the affected tissues, leading to hyper-production of mucus.
However, when the gene was switched off inflammation and excessive mucus production did not occur.
And mice lacking SPDEF were unable to increase mucus production or develop goblet cells.
Further analysis showed that SPDEF plays a complex role switching other genes involved in inflammation and mucus production on and off.
The researchers hope it will be possible to develop treatments that influence activity of the gene, but warn tests in humans are still several years away.
Journal of Clinical Investigation
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First Publishe September 2009
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