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How Your Lungs Protect Themselves

Study resolves paradox about immune response in airways


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THURSDAY, Oct. 2 (HealthDayNews) -- A single class of molecules serves as the immune system's gatekeeper in the lungs, reducing immune response in some situations and encouraging it in other cases.

So finds a study in the Oct. 3 issue of Cell.

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The finding by researchers at National Jewish Medical and Research Center resolves an apparent paradox that had left scientists scratching their heads about how these molecules -- called collectins -- function.

"The lung collectins can effectively discriminate between conditions in the lung that warrant an immune response and those that do not," researcher Peter Henson, a pediatrics professor, says in a news release.

"They do this with a clever mechanism, inhibiting the immune response with one end of their structure and promoting it with the other," Henson says.

Recent research found that mice engineered to lack the lung collectins -- known as surfactant proteins A and D -- showed an enhanced inflammatory response. On the other hand, mice engineered to overexpress the lung collectins had reduced inflammatory response.

In their study, Henson and his colleagues resolved this paradox and revealed the dual role of the lung collectins. They found that one end of the lung collectins binds to a molecule on lung cells that suppresses inflammation.

At the same time, lung collectins are able to recognize and bind to fragments of foreign microorganisms. When that happens, the other end of the lung collectins bind to receptors on the cells that promote inflammation.

"Lung collectins play not one role, but two as they protect the lung not only from harmful pathogens, but also from harmful overreaction by the immune system," Henson says.

More information

Here's where you can learn more about the immune system (www.niaid.nih.gov).



--Robert Preidt

Copyright © 2003 ScoutNews, LLC. All rights reserved.
Last updated 10/2/2003

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SOURCE: National Jewish Medical and Research Center, news release, Oct. 1, 2003


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