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Articles in PresS, published online ahead of print August 16, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00186.2002
Submitted on June 12, 2002
Accepted on August 8, 2002
, in vitro and in vivo
1 Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA; Pediatrics, Baylor College of Medicine, Houston, Texas, USA
2 Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA
3 Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA
4 Department of Pediatrics, Baylor College of Medicine, Houston, Texas, USA
5 Department of Pediatrics, Ajou University, Suwon, Korea, Republic of
6 Department of Pediatrics, Children's Research Institute, Columbus, Ohio, USA
* To whom correspondence should be addressed. E-mail: fdemayo{at}bcm.tmc.edu.
Interferon 
(IFN-), a potent cytokine inducing a wide range of immunologic activities, is increased in the airway secondary to viral infection or during an inflammatory response. This increase in IFN- concentration may alter the expression of specific airway epithelial cell genes that regulate adaptation of airway inflammatory responses. One protein that IFN- induces is the Clara cell secretory protein (CCSP), which may contribute to the attenuation of airway inflammation. This study was done to investigate the molecular mechanism by which IFN- stimulates the expression of the CCSP gene in mouse transformed Clara cells (mtCC) and transgenic mice. Deletion mapping and linker scanner mutations demonstrated that IFN- induced expression of CCSP was regulated, in part, at the level of transcription. In vitro and in vivo studies verified that the minimal IFN- responsive segment was localized to the proximal 166 base pairs of the 5' flanking region. Additionally, IFN- induced expression of CCSP was mediated indirectly through interferon regulatory factor-1 (IRF-1) mediated increase in HNF-3ß.
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