to be linked to abnormal cytokine signaling rather than to a change in cytokine production. Also, the abnormality appears to be localized to a cellular pathway that was not supposed to be part of this disease. Reprogramming of these controls for epithelial immune-response genes helps explain several missing pieces of the asthma story."

In this regard, Holtzman says, the findings offer the first example linking abnormal behavior of JAK/STAT pathways for cytokine signaling to the development of an inflammatory disease.

Activation of the JAK/STAT pathway appears to be fundamental to asthma, Holtzman says, because it was seen in all of the asthmatic subjects regardless of whether they had allergies or were taking corticosteroids, which suppress allergic symptoms.

Holtzman's previous work has suggested a way to dampen the JAK/STAT pathway and hopefully to alleviate asthma. He and his colleagues discovered that adenovirus, which causes respiratory infections, can sabotage the airway cells' inflammatory response by preventing Stat1 from activating genes. So an aerosol of genetically altered adenovirus that could stop asthma without compromising immunity might be a potential therapy. "The virus has taken advantage of us," Holtzman says, "so perhaps we could take advantage of the virus."

Grants from the National Institutes of Health and the Alan A. and Edith L. Wolff Charitable Trust supported this research.

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Contact: Linda Sage
sage@medicine.wustl.edu
314-286-0119
Washington University School of Medicine
28-Apr-1999

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