Effect of Cytokines on Expression of Intercellular Adhesion Molecule - 1 in Nasal Epithelial Cells.
- Author:
Sung Kwang KIM
;
Ho Sun PARK
;
Yong Dae KIM
;
Sang Gyung KIM
- Publication Type:Original Article
- Keywords:
human nasal epithelial cells;
ICAM-l;
IFN-r;
IL-4
- MeSH:
Adhesives;
Asthma;
Cells, Cultured;
Cytokines*;
Endothelial Cells;
Epithelial Cells*;
Fluorescence;
Humans;
Inflammation;
Integrins;
Intercellular Adhesion Molecule-1;
Interleukin-4;
Keratins;
Lymphocyte Function-Associated Antigen-1;
Mast Cells;
Monocytes;
Mucous Membrane;
Nasal Mucosa;
Rhinitis;
Turbinates;
Vimentin;
von Willebrand Factor
- From:Korean Journal of Immunology
1997;19(1):135-144
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Intexcellular adhesion molecule-10CAM- 1) is an important moleade in aehating immune and inflammatory responses. It is found on the surface of hematopoietic and nonhematopoietic cells. It can act as an adhesive ligand for integrins such as LFA-1 (CD1&/CD11a) and MAC-1 (CD18/ CD11b). ICAM-1 is basally expressed in sigaificant amount on a limited number of cell types, including monocytes and endothelial ceRs. But it is inducible or upregulated by INF-r, IL-1p and TNF-a on many cell types. IL-4, a pleiotropic cytokine and mast cell differentiation factor, is upregulated in human allergic disease and stimulates expression of vascular adhesion molecule-1 (VCAM-1) in endothelial cells. IL-4 also promotes expression of surhce ICAM-1 in human mast cells and dermal fidroblasts. So in allergic rhinitis and asthma, IL-4 may be an important cytokine implicated in the pathogenesis of inflammation. We studied the effect of INF-r and IL-4 on expression of ICAM-1 in human nasal epithelial cells (HNEC). HNEC were prepared by primary culture method of monolayer culture of dissociated cells hom human inferior nasal turbinate mucosa. Nasal mucosa were obtained by partial turbinectomy of septal deviation patients. Primary cultured cells were charaterized as an epithelial cell type by indirect immuno-fluorescence assay using antilmdies against cytokeratin-pan, cytokeratin No. 8, vimentin and von Willebrand factor. Using fluorescence activated cell sorter (Coulter EI1TE), we analyzed the quantitative expression of ICAM-1 on HNEC. Treatment of HNEC with IFN-r (1ng/ml) for 24 hours caused about 8 fold increase of the surface ICAM-1 compared with constitutive expression by mean fluorescence intensity (MIF) but IL-4 had little effect. Theses foundings suggest that IFN-r is a potent ICAM-1 inducer in HNEC and further studies are necessary for the role of IL-4 on HNEC.
