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Mechanisms That Potentially Underlie Virus-Induced Exaggerated Inflammatory Responses By Airway Epithelial Cells*

René Lutter, PhD; Matthijs van Wissen, MSc; Thierry Roger, PhD; Paul Bresser, MD, PhD; Koen van der Sluijs, MSc; Monique Nijhuis, PhD; Henk M. Jansen, MD, PhD
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*From the Departments of Pulmonology (Drs. Lutter, Roger, Bresser, and Jansen), Experimental Immunology (Mr. van Wissen), and Experimental Internal Medicine (Mr. van der Sluijs), Academic Medical Center, University of Amsterdam, the Netherlands; and the Department of Virology (Dr. Nijhuis), Eijkman-Winkler Institute, University Medical Center, Utrecht, the Netherlands.

Correspondence to: René Lutter, PhD, Academic Medical Center, Departments of Pulmonology and Experimental Immunology, G1-140, Meibergdreef 9, PO Box 22700, 1100 DE Amsterdam, the Netherlands; e-mail: r.lutter@amc.uva.nl



Chest. 2003;123(3_suppl):391S-392S. doi:10.1378/chest.123.3_suppl.391S
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Many of the proteins that we tend to measure in asthma as indicators of airway inflammation (eg, interleukin [IL]-6, IL-8, granulocyte-macrophage colony-stimulating factor, intercellular adhesion molecule-1, c-jun, and c-fos) or of pathophysiology (eg, endothelin-1, β-adrenergic receptor, glucocorticoid receptor, and inducible nitric oxide synthetase) have in common that their encoding messenger RNA (mRNA) is targeted for rapid degradation. This facilitated degradation ensures that mRNA and, thus, protein expression are limited, which is a crucial regulatory mechanism given that most of these labile mRNAs encode for proteins that can initiate and direct, or redirect, responses. Illustrative in this context is that mice in which the proinflammatory mediator IL-6 was overexpressed in the airway epithelium developed major airway pathology.1 Not surprisingly, therefore, mRNA degradation is strictly regulated, involving complex activation cascades and a range of mRNA-binding proteins.

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