Allergy · 1997 · 45 citations · 34 references
Life SciencesCell BiologyImmunologyCell AdhesionCellular ImmunologyInflammationCytokine BiologyCytokine SignalingInflammatory Cell ResponsesInflammatory SignalingLeukocyte AdhesionOcular InflammationConstitutive Gene ExpressionEpithelial Cell InteractionsEpithelial-derived CytokinesIntercellular Adhesion Molecule 1Proinflammatory Mediators
The expression of intercellular adhesion molecule-1 (CD54 or ICAM-1) on epithelial cells during acute or chronic inflammation may favor the interaction between epithelial cells and leukocytes expressing the natural ligands of ICAM-1, LFA-1 (CD11a/CD18), and Mac-1 (CD11b/CD18). We have evaluated in vitro the expression of ICAM-1 by a conjunctival (WK) and an intestinal (I407) human continuous epithelial cell line. Cells were cultured for 24 h in the presence or absence of IFN-gamma, TNF-alpha, IL-1 beta, IL-4, IL-6, IL-8, IL-10, and TGF-beta 1. Both epithelial cell lines showed a constitutive expression of ICAM-1. IFN-gamma at 500 U/ml and TNF-alpha at 200 ng/ml upregulated ICAM-1 expression; IL-1 beta at 100 pg/ml upregulated ICAM-1 on WK cells only. Cells cultured in the presence of both IFN-gamma and TNF-alpha exhibited a mean fluorescence intensity far greater than those cultured with IFN-gamma or TNF-alpha alone. I407 and WK cells were able to release soluble ICAM-1. IFN-gamma and TNF-alpha enhanced the release of sICAM-1. IL-4, IL-6, IL-8, IL-10, and TGF-beta 1 did not affect either ICAM-1 expression or sICAM-1 release. In conclusion, continuously cultured human epithelial cells may express ICAM-1 on their surface and release it in culture medium. These phenomena are upregulated by proinflammatory cytokines.
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In situ hybridization; a practical approach
International Journal of Biochemistry · 1993 · 1.2K citations
Intercellular Adhesion Molecule-1 (ICAM-1) in the Pathogenesis of asthma
Craig D. Wegner, Robert H. Gundel, Patricia L. Reilly et al. · Science · 1990 · 907 citations