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Effect of cytokines on ICAM‐1 and ZO‐1 expression on human airway epithelial cells
Author(s) -
Relova AnneJacqueline,
Shahana Shahida,
Makeeva Natalia,
Roomans Godfried M.
Publication year - 2005
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2005.05.002
Subject(s) - respiratory epithelium , microbiology and biotechnology , biology , cytokine , apoptosis , epithelium , cell culture , icam 1 , intracellular , viability assay , immunology , biochemistry , genetics
The presence of adhesion molecules on airway epithelial cells may be important in recruiting leukocytes to the epithelium. The study aimed at investigating the effects of interleukin (IL)‐4, IL‐8, IL‐13 and interferon‐γ (IFN‐γ) on cell viability and intracellular adhesion molecule (ICAM)‐1 and zonula occludens protein (ZO)‐1 expression on cultured human basal and columnar airway epithelial cells. Cycloheximide (CHX) induced cell death in both cell lines. The cytokines IL‐4, IL‐8, IL‐13 and IFN‐γ had only minor effects on cell proliferation in the columnar 16HBE14o‐cells, and inhibited the effects of CHX on cell death. IFN‐γ increased ICAM‐1 expression in both cell lines. Western blot analysis showed that CHX inhibited both ICAM‐1 and ZO‐1 expression in the basal cell line. A combination of IL‐4 and IFN‐γ appeared to break the tight junctions. IL‐4 and IL‐13 potentiated CHX‐induced apoptosis in basal cells but not in columnar cells, possibly due to low levels of the IL‐4 receptor. It is concluded that cytokines produced by airway epithelium may have a role in regulating sequestering of leukocytes to the airways during airway inflammation.