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Effect of nickel on the activation state of normal human keratinocytes through interleukin 1 and intercellular adhesion molecule 1 expression
Author(s) -
GUÉNICHE A.,
VIAC J.,
LIZARD G.,
CHARVERON M.,
SCHMITT D.
Publication year - 1994
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.1994.tb08500.x
Subject(s) - intracellular , intercellular adhesion molecule 1 , adhesion , microbiology and biotechnology , nickel , cell adhesion molecule , intercellular adhesion molecule , molecule , chemistry , interleukin , expression (computer science) , biophysics , materials science , immunology , medicine , cell adhesion , biology , cytokine , composite material , computer science , organic chemistry , programming language
Summary Patch tests with nickel on sensitive subjects induce a characteristic allergic reaction involving epidermal and dermal cells, as well as modulation of cytokines and adhesion molecule production. In order to gain further insight into the role of keratinocytes in this phenomenon, we assessed their activation state induced by Ni 2+ by studying interleukin 1 (IL‐1) production and intercellular adhesion molecule 1 (ICAM‐1) expression, using normal human keratinocytes cultured in defined medium. In comparison with controls, the addition of subtoxic NiSO 4 concentrations (0.1–20 μg/ml) to keratinocyte cultures induced a significant, but low release of IL‐1α and IL‐1β at 24 and 48 h, detectable by enzyme‐linked immunosorbent assay of the supernatants of treated cells, Moreover, IL‐1 receptor antagonist was significantly increased in the supernatants and the cell extracts. Using fluorescence‐activated cell sorter analysis, ICAM‐1 expression at 24h was found to be induced in a dose‐dependent manner, reaching a level comparable with that obtained upon interferon‐γ (10 IU/ml) stimulation. Overall, these data confirm the existence of direct interactions between Ni 2+ and keratinocytes, which generate immunological signals of major importance in the pathophysiology of allergic contact dermatitis.