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

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Abstract
SPECIFIC AIMSVirus infections (mostly rhinoviruses) are the major cause of exacerbations of airway disease. Intercellular adhesion molecule-1 (ICAM-1) is a cell surface glycoprotein involved in leukocyte trafficking and recruitment to sites of inflammation; it is also the cellular receptor for 90% of rhinovirus serotypes. Its expression in bronchial epithelium is increased by rhinovirus infection both in vivo and in vitro, making it a pivotal mediator of virus-induced inflammation in the respiratory tract. To investigate a potential role for antioxidants in reducing virus-induced inflammation, we investigated whether reducing agents inhibit in a dose-dependent manner rhinovirus-induced ICAM-1 up-regulation and mRNA induction in primary bronchial or A549 respiratory epithelial cells. We investigated whether reducing agents inhibit rhinovirus-induced ICAM-1 promoter and NF-κB activation. Furthermore, we analyzed whether rhinovirus infection increases oxidant production within airway epithelial cells. These ...
Funding Information
  • Deutsche Forschungsgemeinschaft (405/5 (KD))