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Transepithelial migration of activated eosinophils induces a decrease of E‐cadherin expression in cultured human nasal epithelial cells
Author(s) -
Noriko Kobayashi,
Nobuhisa Terada,
Nanako Hamano,
Tsutomu Numata,
Akiyoshi Konno
Publication year - 2000
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1046/j.1365-2222.2000.00827.x
Subject(s) - eosinophil , degranulation , epithelium , respiratory epithelium , immunofluorescence , immunology , interleukin 8 , microbiology and biotechnology , mucous membrane of nose , inflammation , biology , pathology , medicine , antibody , receptor , asthma , biochemistry
Background The damage of respiratory epithelium in allergic diseases has a close correlation with the extent of eosinophil infiltration. It seems to be a good possibility that eosinophil infiltration could induce the changes in the expression of the epithelial cell adhesion molecules, which play a key role in the maintenance of structural and functional rigidity of epithelium. Objective We observed the expression of E‐cadherin in cultured human nasal epithelial cells (HNECs) to study whether could it be affected by transepithelial migration of inflammatory cells, especially eosinophils. Methods In vitro study of the transmigration assay was designed using various types of inflammatory cells and HNEC monolayers. Various assays of each experimental group were done under the stimulation of interleukin‐5 (IL‐5) and/or platelet activating factor (PAF). Subsequently immunohistochemistry for E‐cadherin was performed in the HNECs. The intensity of immunofluorescence of E‐cadherin was quantified using confocal laser scanning microscopy (CLSM) system and compared before and after the transmigration. Results The mean intensity of immunofluorescence for E‐cadherin decreased significantly after the transmigration of any types of inflammatory cells. Above all, the migration of eosinophils treated with IL‐5 and PAF had an eminent effect on the decrease, whereas the degranulation extracts derived from eosinophils activated by IL‐5 and secretory IgA (sIgA) did not affect the intensity. Conclusion This work suggests that transepithelial migration of inflammatory cells can directly induce the decrease in epithelial E‐cadherin expression. Furthermore, the most prominent change was induced by transmigration of activated eosinophils, which might be caused by some mechanisms independent of the eosinophil contents. The decrease in E‐cadherin expression may trigger the damage of epithelial barrier, which contributes to the pathogenesis of allergic diseases.