Impaired airway epithelial cell responses from children with asthma to rhinoviral infection

• DOI: 10.1111/cea.12767
• Publication Date: 2016-05-30T07:56:42Z
• Authors: A. Kicic; P. T. Stevens; E. N. Sutanto; E. Kicic‐Starcevich; K.‐M. Ling; K. Looi; K. M. Martinovich; L. W. Garratt; T. Iosifidis; N. C. Shaw; A. G. Buckley; P. J. Rigby; F. J. Lannigan; D. A. Knight; S. M. Stick
• Keywords: Rhinovirus

Summary Background The airway epithelium forms an effective immune and physical barrier that is essential for protecting the lung from potentially harmful inhaled stimuli including viruses. Human rhinovirus ( HRV ) infection a known trigger of asthma exacerbations, although mechanism by which this occurs not fully understood. Objective To explore relationship between apoptotic, innate inflammatory responses to in epithelial cells AEC s) obtained children with non‐asthmatic controls. In addition, test hypothesis aberrant repair asthmatics further dysregulated infection. Methods Airway brushings were 39 asthmatic 36 children. Primary cultures established exposed 1b 14. Virus receptor number, virus replication progeny release determined. Epithelial cell apoptosis, IFN ‐β production, cytokine wound proliferation also measured. Results was greater but related number receptors. children, dampened reduced production increased production. inhibited capacity isolated exaggerated defective response seen asthmatics. Addition restored suppressed improved did reduce Conclusions Collectively, delays inhibits apoptotic processes delayed only partially reversed exogenous ‐β.