Published ahead of print on September 29, 2005, doi:10.1165/rcmb.2005-0338OC Am. J. Respir. Cell Mol. Biol., Volume 34, Number 1, January 2006, 119-127 A more recent version of this article appeared on January 1, 2006
Submitted on September 2, 2005 (R)-Albuterol Elicits Anti-Inflammatory Effects in Human Airway Epithelial Cells via iNOSBrian N Chorley1,1 Department of Molecular Biomedical Sciences, North Carolina State University, College of Veterinary Medicine, Raleigh, NC, USA, 2 Department of Molecular Biomedical Sciences, North Carolina State University, College of Veterinary Medicine, Raleigh, NC, USA; Tanox, Inc., Houston, TX, USA, 3 Department of Molecular Biomedical Sciences, North Carolina State University, College of Veterinary Medicine, Raleigh, NC, USA; Department of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, NC, USA * To whom correspondence should be addressed. E-mail: kenneth_adler{at}ncsu.edu.
Catecholamines can suppress production of inflammatory mediators in different cell types, including airway epithelium, but downstream signaling mechanisms involved in regulation of these anti-inflammatory effects are largely unknown. We theorized that acute
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2-adrenergic stimulation of airway epithelial cells with albuterol could suppress production and release of inflammatory mediators, specifically granulocyte macrophage colony stimulating factor (GM-CSF) via a pathway involving inducible nitric oxide synthase (iNOS). Normal human bronchial epithelial (NHBE) cells in primary culture were exposed to a cytokine mixture (10 ng/ml each interferon-
and interleukin- 1
isoform, was required for iNOS message increase, but protein kinases A and G were not involved in the pathway. Overall, this study identifies a novel pathway by which 
