The Expression of ICAM-1 by Cytokines and the Effect of Dexamethasone on ICAM-1 Expression in Cultured Keratocytes.
- Author:
Ho Bum KIM
1
;
Hungwon TCHAH
Author Information
1. Department of Ophthalmology, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
ICAM-1;
Keratocyte;
Cytokines;
Dexamethasone;
Immunocytochemical study
- MeSH:
Cornea;
Corneal Diseases;
Cytokines*;
Dexamethasone*;
Enzyme-Linked Immunosorbent Assay;
Glycoproteins;
Inflammation;
Intercellular Adhesion Molecule-1*;
Leukocytes;
Transforming Growth Factor beta;
Tumor Necrosis Factor-alpha
- From:Journal of the Korean Ophthalmological Society
1999;40(7):1755-1762
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Intercellular adhesion molecule-1 (ICAM-1) Is a cell-surface glycoprotein that may regulate leukocyte-endothelial adhesion, leukocyte migration into the tissues, and leukocyte trafficking with target cells during inflammation and immune responses. Expression of ICAM-1 have been observed in diseased cornea, and it has been reported that expression on corneal cells is increased in the presence of pro-inflammatory cytokines. We investigated expression of ICAM-1 by various cytokines on cultured rabbit keratocytes and effect of dexamethasone on cytokine-induced ICAM 1 expression, using an ELISA technique. Cultured rabbit keratocytes were incubated for 24hrs with INF-gamma 10ng/ml, TNF-alpha 10ng/ml IL-1beta 5ng/ml, TGF beta 5ng/ml, with or without 0.1micromiter Dexamethasone. Rabbit keratocytes treated with cytokine or dexamethasone were incubated with antral-ICAM-1 for 15 hours. Expression of ICAM-1 was measured with ELISA technique. As a result, expression of ICAM-1 was increased in rabbit keratocytes stimulated with INF-gamma, TNF-alpha, TGF-beta, not IL-1beta, and dexamethasone inhibited expression of ICAM-1 in cells stimulated with INF-gamma, TNF-alpha. This results are helpful to understand the role of ICAM-1 in the pathophysiology of inflammatory corneal diseases and the action mechanism of glucocorticosteroids. Further study about expression of ICAM-1 and their regulation & modulation may lead to new therapies in treating inflammatory corneal diseases.
