Iron Chelation Attenuates LPS-Induced IL-6 Release in Cystic Fibrosis Epithelial Cells

Of all the deadly genetic diseases, cystic fibrosis (CF) is the most common one affecting Canadian children and young adults. CF results from a genetic change in a protein called CFTR (CF transmembrane conductance regulator). In the lungs, this protein has the role of making sure salts and fluids easily come in and out of cells to form a protective mucous barrier against germs. In CF patients however, because the CFTR protein is not functioning properly, the mucous barrier becomes thick and viscous which is an ideal environment for bacteria to grow and makes the lung chronically inflammed. The goal of my research is to remove excess iron present at the surface of the lung to reduce the inflammation and prevent further damage from bacterial infection. For this, I am studying how cells from CF patients respond to treatment with a novel molecule called DIBI that has already shown promises in reducing lung inflammation. Our findings will inform further research to develop therapeutic treatments for the lung of CF patients.