Transepithelial migration of activated eosinophils induces a decrease of E-cadherin expression in cultured human nasal epithelial cells.
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.


CONCLUSIONS
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.
Kobayashi
N
N
Department of Otorhinolaryngology, School of Medicine, Chiba University, Chiba City, Chiba, Japan.
Terada
N
N
Hamano
N
N
Numata
T
T
Konno
A
A
D000293:Adolescent; D000328:Adult; D015820:Cadherins / Q000378:metabolism*; D002465:Cell Movement; D002478:Cells, Cultured; D004804:Eosinophils / Q000276:immunology*; D004847:Epithelial Cells / Q000276:immunology / Q000378:metabolism*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D015848:Interleukin-5 / Q000494:pharmacology; D008297:Male; D018613:Microscopy, Confocal; D009297:Nasal Mucosa / Q000166:cytology / Q000378:metabolism*; D010972:Platelet Activating Factor / Q000494:pharmacology; D012221:Rhinitis, Allergic, Perennial / Q000276:immunology / Q000503:physiopathology
D015820:Cadherins; D015848:Interleukin-5; D010972:Platelet Activating Factor