Co-infection with HRV and Pseudomonas aeruginosa Modulates Beta-Defensin-2 Expression from the Airway Epithelium
Abstract
Respiratory infections are the most common triggers of acute exacerbations of chronic obstructive pulmonary disease (COPD), with human rhinovirus (HRV) and Pseudomonas aeruginosa being two common pathogens detected. Human beta-defensin (HBD)-2 is an antimicrobial peptide that plays an integral role in the innate defense response to infection. Here, we sought to determine how co-infection of airway cells with HRV and P. aeruginosa modulates HBD2 expression, and whether the normal HBD2 response to co-infections are altered in COPD subjects compared to healthy non-smokers. Synergistic increases in HBD2 from the airway epithelium were seen with the combination HRV and P. aeruginosa compared to either treatment alone. This synergistic response was dependent on flagellin acting through the TLR5 pathway. Finally, a reduction in HBD2 was observed in epithelial cells obtained from patients with COPD compared to cells from non-smokers following HRV and P. aeruginosa co-infection.
Description
Keywords
Immunology
Citation
Arnason, J. (2015). Co-infection with HRV and Pseudomonas aeruginosa Modulates Beta-Defensin-2 Expression from the Airway Epithelium (Master's thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca. doi:10.11575/PRISM/25350