IL-1 ALPHA-INDUCED EXPRESSION OF ICAM-1 ON CULTURED HYPERPROLIFERATIVE KERATINOCYTES: SUPPRESSION BY ANTIPSORIATIC DIMETHYL-FUMARATE
| Autor: | Bernd Bonnekoh, Gustav Mahrle, Bela Sebök |
|---|---|
| Rok vydání: | 1994 |
| Předmět: |
Keratinocytes
Dimethyl Fumarate medicine.medical_treatment Alpha (ethology) Dermatology chemistry.chemical_compound Fumarates Gene expression Humans Psoriasis Medicine Cells Cultured Dose-Response Relationship Drug Dimethyl fumarate business.industry Intercellular Adhesion Molecule-1 Molecular biology Dose–response relationship HaCaT medicine.anatomical_structure Cytokine chemistry Immunology Systemic administration business Keratinocyte Cell Adhesion Molecules Interleukin-1 |
| Zdroj: | International Journal of Dermatology. 33:367-370 |
| ISSN: | 1365-4632 0011-9059 |
| DOI: | 10.1111/j.1365-4362.1994.tb01070.x |
| Popis: | Background In the psoriatic plaque both IL-1 dysregulation and ICAM-1 expression on keratinocytes have been previously described. Furthermore systemic administration of fumarates has been reported to be effective in psoriasis. We, therefore, studied the effect of dimethyl-fumarate ester (DMF) on the putative IL-1-induced ICAM-1 expression. Methods Hyperproliferative human keratinocytes (HaCaT cell line) were incubated in 10 to 100 U/mL IL-1 alpha for 24 h with and without preincubation with 0.4-12.0 microM DMF: Expression of ICAM-1 was measured by a special ELISA-APAAP technique. Results The exposure to IL-1 led to a significant dose-dependent induction of ICAM-1 expression of from 124 +/- 17 to 194 +/- 22% (control 100 +/- 12%), while proliferation remained unaltered. Pretreatment with > or = 4 microM DMF resulted in a distinct suppression of ICAM-1 expression and a slight decrease in proliferation. Conclusions The present results show that ICAM-1 expression on hyperproliferative keratinocytes may be triggered by IL-1 alpha and serve as a molecular target for antipsoriatic DMF. |
| Databáze: | OpenAIRE |
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