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Mediators of Inflammation
Volume 2016, Article ID 9798206, 7 pages
Research Article

Th17 Cytokines Disrupt the Airway Mucosal Barrier in Chronic Rhinosinusitis

1Department of Surgery (Otorhinolaryngology Head and Neck Surgery), The Queen Elizabeth Hospital and The University of Adelaide, Adelaide, SA 5011, Australia
2School of Biology, Faculty of Science and Engineering, Flinders University of South Australia, Adelaide, SA 5042, Australia

Received 1 October 2015; Revised 23 December 2015; Accepted 27 December 2015

Academic Editor: Kong Chen

Copyright © 2016 Mahnaz Ramezanpour et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cytokine mediated changes in paracellular permeability contribute to a multitude of pathological conditions including chronic rhinosinusitis (CRS). The purpose of this study was to investigate the effect of interferons and of Th1, Th2, and Th17 cytokines on respiratory epithelium barrier function. Cytokines and interferons were applied to the basolateral side of air-liquid interface (ALI) cultures of primary human nasal epithelial cells (HNECs) from CRS with nasal polyp patients. Transepithelial electrical resistance (TEER) and permeability of FITC-conjugated dextrans were measured over time. Additionally, the expression of the tight junction protein Zona Occludens-1 (ZO-1) was examined via immunofluorescence. Data was analysed using ANOVA, followed by Tukey HSD post hoc test. Our results showed that application of interferons and of Th1 or Th2 cytokines did not affect the mucosal barrier function. In contrast, the Th17 cytokines IL-17, IL-22, and IL-26 showed a significant disruption of the epithelial barrier, evidenced by a loss of TEER, increased paracellular permeability of FITC-dextrans, and discontinuous ZO-1 immunolocalisation. These results indicate that Th17 cytokines may contribute to the development of CRSwNP by promoting a leaky mucosal barrier.