IκBζ is constitutively expressed in human and murine airway epithelium

AIM: IκBζ is a transcriptional factor induced in immune cells upon Toll-like receptor activation. Recent studies demonstrated unconventional, constitutive expression of IκBζ in epithelium of mouse skin and eyes, possibly reflecting continuous activation of TLRs by pathogen-associated molecular patterns. In this context, another mucosal surface, the lung epithelium, may not be as actively exposed to the external environment as skin and eyes, especially since the lower airways are conceived to be sterile. Whether IκBζ expression in the lungs is constitutive or induced remains unexplored. SIGNIFICANCE: IκBζ is linked to lung disorders due to its vital role in regulating protective cytokines and antimicrobial peptides in airway epithelium and can therefore be a potential biomarker and a candidate for therapy. METHODS: We evaluated IκBζ expression in airway epithelia of healthy humans and three kinds of mice: normal, gnotobiotic and partial Nfkbiz knockout, using immunostaining and western blotting with antiserum raised against recombinant IκBζ in our laboratory. RESULTS: We observed positive signal in the nuclei of ciliated epithelial cells lining the central airways in healthy humans and normal mice. Airway cells from gnotobiotic mice also stained positive, suggesting that IκBζ expression does not require induction by PAMPs. We also observed staining in the lung epithelia from partial Nfkbiz knockout mice, showing specificity of antiserum to IκBζ. Furthermore, immunoblotting tissue homogenates from gnotobiotic mouse lungs and primary human airway epithelial cells confirmed constitutive IκBζ expression. CONCLUSIONS: Our data demonstrates constitutive expression of IκBζ protein in airway epithelium, indicating a role for this molecule in lung homeostasis.