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The FASEB Journal, Vol 8, 1081-1087, Copyright © 1994 by The Federation of American Societies for Experimental Biology

RESEARCH COMMUNICATIONS

Interleukin-1 alpha mediates phorbol ester-induced inflammation and epidermal hyperplasia

WY Lee, MF Lockniskar and SM Fischer
Division of Pharmacology/Toxicology, College of Pharmacy, University of Texas at Austin 78712.

The topical application of the tumor promoter 12-O-tetradecanoylphorbol- 13-acetate (TPA) to murine skin produces acute inflammatory and hyperplastic responses that have been associated with the promotion stage of skin carcinogenesis. It has been shown in a previous study that TPA induces the expression of the highly inflammatory cytokine, interleukin (IL) -1 alpha, in the epidermis of SENCAR mice. The goal of this study was to investigate the role of IL-1 alpha in several TPA- induced responses in skin. Topical application of TPA (1 microgram) enhanced the production of immunoreactive IL-1 alpha protein, primarily associated with the suprabasal keratinocytes. IL-1 alpha intradermally injected in the dorsal surface significantly increased (P < 0.001) vascular permeability at low concentrations (1-1000 microU) and increased (P < 0.001) inflammatory cell infiltration and epidermal hyperplasia at higher concentrations (10(3) U). TPA produced fourfold increases in vascular permeability as measured by Evans blue dye leakage; this effect was prevented by intradermal injection of anti-IL- 1 alpha antibody (25-75 micrograms). Furthermore, injected anti-IL-1 alpha antibody significantly reduced (P < 0.001) TPA-induced inflammatory cell infiltration and epidermal hyperplasia. This study suggests that IL-1 alpha directly or indirectly mediates the inflammatory and hyperplastic responses elicited by topical treatment with TPA.


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Copyright © 1994 by The Federation of American Societies for Experimental Biology.