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Toxicology. 1998 Aug 21;129(2-3):193-200.

Selective induction of cell-associated interleukin-1alpha in murine keratinocytes by chemical allergens.

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  • 1Center for Cosmetic Toxicology, Institute of Pharmacological Sciences, University of Milan, Italy. emanuela.corsini@unimi.it

Abstract

Cytokines may be useful tools to discriminate between irritant and allergic contact dermatitis. In the mouse only, it has been demonstrated by other, that contact sensitizers up-regulated keratinocytes-derived interleukin-1alpha (IL-1), macrophage inflammatory protein-2 and interferon induced protein 10 mRNAs. The purpose of this study was to investigate the possibility to use in vitro IL-1 production by a murine keratinocyte cell line for preliminary screening of chemicals for their irritant and/or allergic potential. We investigated the effects of five relevant skin allergens (dinitrochlorobenzene, oxazolone, nickel sulfate, penicillin G and eugenol), two skin irritants (benzalkonium chloride, and methylsalicilate) and two compounds with no sensitizing activity (glycerol and ethanol) on IL-1 production in HEL30 cells. Twenty four hours following treatment, both IL-1 release in conditioned media and cell-associated IL-1 were measured by a specific sandwich ELISA. Under our experimental conditions, only contact sensitizers were able to increase in a dose dependent fashion cell-associated IL-1, confirming the in vivo findings. Both skin irritants and allergens induced the release of IL-1, because of the irritative properties of both chemicals, while ethanol and glycerol failed to induce changes in IL-1 production, confirming the specificity of the proposed test. Taken together, these data indicate that it may be realistic to consider potential skin allergens those chemicals which are able to increase cell-associated IL-1, to consider skin irritants those chemicals which induce only IL-1 release, and to exclude as potential allergens or irritants those chemicals which fail to induce changes in IL-1 production.

PMID:
9772097
[PubMed - indexed for MEDLINE]
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