CXCL8 and cystic fibrosis: These different cellular redistributions of TLRs render the CF airway epithelial cells more susceptible to host-pathogen interactions between bacterial constituents (pili and flagellin) and the receptors involved in the transduction of “danger signal” at apical membrane, favoring the release of cytokines (as described before in section host-pathogen interactions and intracellular signaling modulating IL-8/CXCL8 expression).