Reducing agents inhibit rhinovirus-induced up-regulation of the rhinovirus receptor intercellular adhesion molecule-1 (ICAM-1) in respiratory epithelial cells

• Published in: The FASEB journal Vol. 16; no. 14; p. 1934
• Main Authors: Papi, Alberto, Papadopoulos, Nikolaos G, Stanciu, Luminita A, Bellettato, Cinzia M, Pinamonti, Silvano, Degitz, Klaus, Holgate, Stephen T, Johnston, Sebastian L
• Format: Journal Article
• Language: English
• Published: United States 01.12.2002
• Subjects: Animals; Cell Line; Cells, Cultured; Dose-Response Relationship, Drug; Glutathione - pharmacology; Intercellular Adhesion Molecule-1 - biosynthesis; Intercellular Adhesion Molecule-1 - genetics; Models, Biological; NF-kappa B - metabolism; Promoter Regions, Genetic; Receptors, Virus - biosynthesis; Receptors, Virus - genetics; Reducing Agents - pharmacology; Respiratory Mucosa - drug effects; Respiratory Mucosa - metabolism; Respiratory Mucosa - virology; Rhinovirus - pathogenicity; RNA, Messenger - biosynthesis; Superoxides - metabolism; Transcriptional Activation; Up-Regulation

Rhinoviruses are the major cause of common colds and of asthma exacerbations. Intercellular adhesion molecule-1 (ICAM-1) has a central role in airway inflammation and is the receptor for 90% of rhinoviruses. Rhinovirus infection of airway epithelium induces ICAM-1. Because redox state is directly im...