Abstract
Respiratory virus infections play an important role in cystic fibrosis (CF) exacerbations, but underlying pathophysiological mechanisms are poorly understood. We aimed at assessing whether an exaggerated inflammatory response of the airway epithelium upon virus infection could explain the increased susceptibility of CF patients towards respiratory viruses.
We used primary bronchial and nasal epithelial cells obtained from healthy control subjects (n=24) and CF patients (n=18). IL-6, IL-8/CXCL8, IP-10/CXCL10, MCP-1/CCL2, RANTES/CCL5 and Gro-α/CXCL1 levels in supernatants and mRNA expression in cell lysates were measured before and after infection with rhinoviruses (RV-16; RV-1B) and RSV. Cytotoxicity was assessed by LDH assay and flow cytometry.
All viruses induced strong cytokine release in both control and CF cells. The inflammatory response upon virus infection was heterogeneous and depended on cell type and virus used, but was not increased in CF compared to control cells. On the contrary, there was a marked trend towards lower cytokine production associated with increased cell death in CF cells.
An exaggerated inflammatory response to virus infection in bronchial epithelial cells does not explain the increased respiratory morbidity after virus infection in CF patients.
- ERS
