Interleukin-4 and interleukin-13 compromise the sinonasal epithelial barrier and perturb intercellular junction protein expression

Int Forum Allergy Rhinol. 2014 May;4(5):361-70. doi: 10.1002/alr.21298. Epub 2014 Feb 7.

Abstract

Background: Altered expression of epithelial intercellular junction proteins has been observed in sinonasal biopsies from nasal polyps and epithelial layers cultured from nasal polyp patients. These alterations comprise a "leaky" epithelial barrier phenotype. We hypothesize that T helper 2 (Th2) cytokines interleukin (IL)-4 and IL-13 modulate epithelial junction proteins, thereby contributing to the leaky epithelial barrier.

Methods: Differentiated primary sinonasal epithelial layers cultured at the air-liquid interface were exposed to IL-4, IL-13, and controls for 24 hours at 37°C. Epithelial resistance measurements were taken every 4 hours during cytokine exposure. Western blot and immunofluorescence staining/confocal microscopy were used to assess changes in a panel of tight and adherens junction proteins. Western blot densitometry was quantified with image analysis.

Results: IL-4 and IL-13 exposure resulted in a mean decrease in transepithelial resistance at 24 hours to 51.6% (n = 6) and 68.6% (n = 8) of baseline, respectively. Tight junction protein junctional adhesion molecule-A (JAM-A) expression decreased 42.2% with IL-4 exposure (n = 9) and 37.5% with IL-13 exposure (n = 9). Adherens junction protein E-cadherin expression decreased 35.3% with IL-4 exposure (n = 9) and 32.9% with IL-13 exposure (n = 9). Tight junction protein claudin-2 showed more variability but had a trend toward higher expression with Th2 cytokine exposure. There were no appreciable changes in claudin-1, occludin, or zonula occludens-1 (ZO-1) with IL-4 or IL-13 exposure.

Conclusion: Sinonasal epithelial exposure to Th2 cytokines IL-4 and IL-13 results in alterations in intercellular junction proteins, reflecting increased epithelial permeability. Such changes may explain some of the phenotypic manifestations of Th2-mediated sinonasal disease, such as edema, nasal discharge, and environmental reactivity.

Keywords: IL-13; IL-4; Th2 inflammation; allergic fungal sinusitis; cytokine; epithelial cell; inflammation; interleukin 13; interleukin 4; rhinosinusitis.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cadherins / genetics
  • Cadherins / metabolism
  • Cell Adhesion Molecules / genetics
  • Cell Adhesion Molecules / metabolism
  • Cell Membrane Permeability
  • Cells, Cultured
  • Claudin-2 / genetics
  • Claudin-2 / metabolism
  • Down-Regulation / immunology
  • Epithelial Cells / physiology*
  • Epithelial Cells / ultrastructure
  • Humans
  • Intercellular Junctions / genetics
  • Intercellular Junctions / metabolism*
  • Intercellular Junctions / pathology
  • Interleukin-13 / immunology*
  • Interleukin-4 / immunology*
  • Microscopy, Confocal
  • Nasal Polyps / immunology*
  • Paranasal Sinuses / pathology*
  • Receptors, Cell Surface / genetics
  • Receptors, Cell Surface / metabolism
  • Th2 Cells / immunology*

Substances

  • Cadherins
  • Cell Adhesion Molecules
  • Claudin-2
  • F11R protein, human
  • Interleukin-13
  • Receptors, Cell Surface
  • Interleukin-4