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IL‐1 ALPHA‐INDUCED EXPRESSION OF ICAM‐1 ON CULTURED HYPERPROLIFERATIVE KERATINOCYTES: SUPPRESSION BY ANTIPSORIATIC DIMETHYL‐FUMARATE
Author(s) -
SEBÖK BELA,
BONNEKOH BERND,
MAHRLE GUSTAV
Publication year - 1994
Publication title -
international journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.677
H-Index - 93
eISSN - 1365-4632
pISSN - 0011-9059
DOI - 10.1111/j.1365-4362.1994.tb01070.x
Subject(s) - hacat , psoriasis , icam 1 , dimethyl fumarate , cell culture , medicine , keratinocyte , alpha (finance) , microbiology and biotechnology , cell growth , cancer research , immunology , biology , biochemistry , cell adhesion molecule , construct validity , genetics , nursing , patient satisfaction , multiple sclerosis
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 kertinocytes (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 uM dmf. Expression of icam‐1 was measured by a special ELISA‐APAAP technique. Results. The exposure to 11‐1 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 > 4 μM DMF resulted in a distinct suppression of ICAM‐1 expression and a slight decrease in proliferation. Conclusions. The present results show that ICAMI‐1 expression on hyperproliferative keratinocytes may be triggered by il‐i alpha and serve as a molecular target for antipsoriatic DMF.