Regulation of dectin-1 in cystic fibrosis bronchial epithelial cells during host pathogen interactions

Cystic fibrosis (CF) lung disease is characterized by chronic infection and inflammation. Studies show that CF airways are frequently colonized with fungi. As a response, innate immune pattern recognition receptors sense the microbial threat and activate the immune response. Dectin-1 is a transmembrane receptor that plays a crucial part in the fungal recognition by host immune cells. It is expressed on myeloid cells, but few reports have described its inducible expression in pulmonary epithelial cell lines. However, the role of these receptors during pathogen recognition in CF lung disease remains incompletely understood. We used in vitro cell culture methods consisting of immortalized human bronchial epithelial (HBE) and cystic fibrosis (CFBE) cell lines and studied the expression and regulation of Dectin-1. The protein expression and localization of Dectin-1 was assessed using Fluorescence activated cell sorting and Immunofluorescence. mRNA levels were quantified using real time quantitative polymerase chain reaction (RT-qPCR). We found that A. fumigatus induced higher intracellular Dectin-1 expression and mRNA in HBE cells, which was reduced in CFBE cells. Dectin-1 mRNA levels were higher and remained unchanged in CFBE cells after A. fumigatus challenge as compared to HBE cells. Localisation studies showed increased Dectin-1 expression after fungal stimulation in HBE cells. The overall expression of Dectin-1 was found to be lower in CFBE cells in comparison to HBE cells. In conclusion, the results shed a light on the biological role of CF bronchial epithelia in innate defence against A. fumigatus infection and the importance of Dectin-1 in this process.