Rhinovirus infection causes steroid resistance in airway epithelium through nuclear factor кB and c-Jun N-terminal kinase activation
Inhaled glucocorticoids are often highly effective in treating symptoms of asthma exacerbations, however they are ineffective at treating and preventing exacerbations brought on by rhinovirus infection, especially in children. Glucocorticoids act by binding to glucocorticoid receptors (GR) α which become activated and translocate to the nucleus, leading to the activation of down-stream anti-inflammatory pathways. Papi et al sought to determine the mechanistic actions of glucocorticoids during rhinovirus infection by studying factors in these anti-inflammatory pathways ( J Allergy Clin Immunol 2013; 132(5): 1075-1085 ). Using a variety of assays and human bronchial epithelial cells, the authors determined that the rhinovirus RV-16 reduces the ability of dexamethasone to inhibit the pro-inflammatory cytokine IL-1β induction of the chemokine CXCL8. They went on to show that there is an RV-16 dependent impairment of dexamethasone-induced GRα nuclear translocation that is m...