There are only a few studies on the influence of inflammation on claudin expression in bronchial cells. In well differentiated human airway epithelial cells (HAE) from cystic fibrosis (CF) and non-CF patients, combined treatment with IL-1β and TNFα led to a decrease in transmembrane potential and tight junctional barrier function, the changes appearing more rapidly in CF cells [37] . In analysis of airway epithelial cells the expression of claudins 1 and 4 were not altered, however, there was a decrease in the protein expression of ZO1 and JAM and upregulation of hyperphosphorylated occludin and ICAM1 [37] . The influence of these cytokines appeared to be mediated by PKC/lambda [37] .