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Interferon-gamma down-regulates claudin-1 and impairs the epithelial barrier function in primary cultured human

S Tedelind1, L E Ericson, J O Karlsson

  • 1Institute of Anatomy and Cell Biology, Sahlgrenska Academy at Göteborg University, Box 420, 40530 Göteborg, Sweden. sofia.tedelind@anatcell.gu.se

European Journal of Endocrinology
|August 29, 2003
PubMed

Insights

Interferon-gamma (IFN-gamma) disrupts the barrier function of human thyroid cells by down-regulating claudin-1. This finding is relevant to autoimmune thyroid diseases and antigen exposure.

Area of Science:

  • Endocrinology
  • Immunology
  • Cell Biology

Background:

  • Proinflammatory cytokines impact follicular epithelium in autoimmune thyroid disease.
  • Interferon-gamma (IFN-gamma) is a key cytokine in autoimmune conditions.

Purpose of the Study:

  • To investigate the effect of IFN-gamma on the barrier function of primary cultured human thyrocytes.
  • To understand the molecular mechanisms underlying IFN-gamma's impact on thyroid epithelial cells.

Main Methods:

  • Primary human thyrocytes from Graves' disease follicles were cultured as polarized monolayers.
  • Transepithelial electrical resistance (TEER) was measured to assess barrier function.
  • Tight junction proteins (claudin-1, occludin) and cell morphology were analyzed via immunofluorescence, Western blotting, and electron microscopy.

Main Results:

  • Thyrotropin (TSH) enhanced epithelial barrier function, increasing TEER.
  • IFN-gamma significantly decreased TEER, indicating barrier disruption.
  • IFN-gamma reduced claudin-1 expression and altered its distribution, without affecting occludin or causing cytotoxicity. TSH could not reverse IFN-gamma's effects.

Conclusions:

  • IFN-gamma impairs the barrier function of human thyroid epithelial cells.
  • The loss of barrier integrity is associated with claudin-1 down-regulation and redistribution.
  • This effect of IFN-gamma may contribute to thyroid autoimmunity by facilitating autoantigen exposure.
Abstract

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