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Channeling efforts to fight cystic fibrosis
Date:9/17/2010

model for studies of human lung function and a valuable tool for elucidating pathology of lung disease in CF," notes Foskett.

The team also discovered that fluid secretion by the mucous cells -- in response to neurotransmitters -- requires CFTR. This secretion was absent in the pigs lacking CFTR. However, the same cells that lacked the CFTR chloride ion channel, mimicking the condition in human CF, expressed another, different chloride ion channel that could be activated by elevating intracellular calcium by the same neurotransmitters. The presence of both channels in the same mucous cells suggests that the calcium-activated chloride channel could be targeted therapeutically to compensate for lack of CFTR functioning channels in CF-harmed cells.

"This crosstalk between the signaling pathways that activate the two different chloride ion channels now gives us a completely new therapeutic strategy to think about," says Foskett. For example, the presence of the calcium-activated chloride channel would enable CF mucous cells to secrete in response to stimulation that would have normally required the CFTR channel. Drugs that could enhance the magnitude of the calcium response might also enable activation of calcium-activated chloride channel-mediated secretion in CF cells. Importantly, such agents might be able to lead to secretion only during times of physiological stimulus, utilizing the appropriate neural regulation of secretion that likely remains intact in CF.


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Contact: Karen Kreeger
karen.kreeger@uphs.upenn.edu
215-349-5658
University of Pennsylvania School of Medicine
Source:Eurekalert  

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