Description:
<jats:sec><jats:label /><jats:p>Psoriasin is a low molecular weight, Ca2+binding protein with antimicrobial activity. Using RT‐PCR and immunoblotting, we determined that psoriasin is expressed in a number of human airway epithelial cells lines. We next investigated physiological and pathophysiological mediators we hypothesised might influence psoriasin expression, specifically comparing the normal human bronchial epithelial cell line 16HBE14o‐ to the CF bronchial epithelial cell line CFBE41o‐. Psoriasin was expressed at much lower levels in the CFBE41o‐ cells compared to non‐CF cells. Treatment with the cytokine IL‐22 significantly upregulated psoriasin expression in the 16HBE14o‐ cells, while there was no effect on the CFBE41o‐ cells. Treatment with the pro‐inflammatory cytokines IFNγ, TNF‐α and IL‐1β also effected psoriasin expression: IFNγ and TNF‐α increased expression in both cell lines, while IL‐1β increased expression in the CFBE41o‐ cells only. Exposure to the oxidant stresser t‐butylhydroperoxide decreased psoriasin expression in normals with no effect on the CF cell line. Finally, inhibition of the CFTR Cl‐ channel also affected psoriasin expression. This is the first evidence of psoriasin expression in human airway epithelia, and suggests that differential responses exist between normal and CF airway cells, potentially contributing to their innate antimicrobial defence. Supported by the Canadian CF Foundation.</jats:p></jats:sec>