Intercellular adhesion molecule‐1 on cultured human epithelial cell lines: influence of proinflammatory cytokines

Paolieri F, Battifora M, Riccio AM, Pesce G, Canonica GW, Bagnasco M. Intercellular adhesion molecule‐1 on cultured human epithelial cell lines: influence of proinflammatory cytokines. The expression of intercellular adhesion molecule‐1 ‘CD54 or ICAM‐1’ on epithelial cells during acute or chronic in...

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Veröffentlicht in:Allergy (Copenhagen) 1997-05, Vol.52 (5), p.521-531
Hauptverfasser: Paolieri, F., Battifora, M., Riccio, A. M., Pesce, G., Canonica, G. W., Bagnasco, M.
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Sprache:eng
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Zusammenfassung:Paolieri F, Battifora M, Riccio AM, Pesce G, Canonica GW, Bagnasco M. Intercellular adhesion molecule‐1 on cultured human epithelial cell lines: influence of proinflammatory cytokines. 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 ‘1407’ human continuous epithelial cell line. Cells were cultured for 24 h in the presence or absence of IFN‐γ, TNF‐α, IL‐1β, IL‐4, IL‐6, IL‐8, IL‐10, and TGF‐Jβ1. Both epithelial cell lines showed a constitutive expression of ICAM‐1. IFN‐γ at 500 U/ml and TNF‐α at 200 ng/ml upregulated ICAM‐1 expression; IL‐1β at 100 pg/ml upregulated ICAM‐1 on WK cells only. Cells cultured in the presence of both IFN‐γ and TNF‐α exhibited a mean fluorescence intensity far greater than those cultured with IFN‐γ or TNF‐α alone. 1407 and WK cells were able to release soluble ICAM‐1. IFN‐γ and TNF‐α enhanced the release of sICAM‐1. IL‐4, IL‐6, IL‐8, IL‐10, and TGF‐β1 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.
ISSN:0105-4538
1398-9995
DOI:10.1111/j.1398-9995.1997.tb02595.x