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Related Experiment Videos

Transepithelial migration of activated eosinophils induces a decrease of E-cadherin expression in cultured human

N Kobayashi1, N Terada, N Hamano

  • 1Department of Otorhinolaryngology, School of Medicine, Chiba University, Chiba City, Chiba, Japan.

Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology
|June 10, 2000
PubMed
Summary

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Inflammatory cell migration, especially activated eosinophils, significantly reduces E-cadherin expression in human nasal epithelial cells (HNECs). This decrease in E-cadherin may contribute to epithelial barrier damage in allergic diseases.

Area of Science:

  • Allergy and Immunology
  • Epithelial Biology
  • Cellular Adhesion

Background:

  • Respiratory epithelium damage in allergic diseases correlates with eosinophil infiltration.
  • Eosinophils may alter epithelial cell adhesion molecule expression, impacting epithelial integrity.

Purpose of the Study:

  • To investigate the effect of inflammatory cell transepithelial migration on E-cadherin expression in cultured human nasal epithelial cells (HNECs).
  • To determine if eosinophil migration specifically impacts E-cadherin levels.

Main Methods:

  • In vitro transmigration assay using HNEC monolayers and various inflammatory cells.
  • Stimulation with interleukin-5 (IL-5) and/or platelet activating factor (PAF).
  • Immunohistochemistry and confocal laser scanning microscopy (CLSM) to quantify E-cadherin immunofluorescence intensity.

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Main Results:

  • Transepithelial migration of all tested inflammatory cells significantly decreased E-cadherin immunofluorescence intensity.
  • Migration of eosinophils treated with IL-5 and PAF showed the most significant reduction in E-cadherin.
  • Eosinophil degranulation extracts did not affect E-cadherin intensity.

Conclusions:

  • Transepithelial migration of inflammatory cells directly reduces epithelial E-cadherin expression.
  • Activated eosinophil migration has a prominent effect on E-cadherin decrease, potentially via mechanisms independent of released contents.
  • Reduced E-cadherin expression may compromise the epithelial barrier, contributing to allergic disease pathogenesis.