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Long-term exposure to UV irradiation and toxic chemicals is associated with chronic inflammation that contributes to skin cancer development with interleukin-1 alpha (IL-1 α ), constitutively produced by keratinocytes, playing a pivotal role in skin inflammation. The aim of this study was to investigate the modulation of IL-1 α  production in the HaCaT keratinocyte cell line. Phorbol 12-myristate 13-acetate failed to induce IL-1 α  in HaCaT cells, and this might be associated with the specific deficiency known to affect downstream signalling of the MEK/ERK pathway in these cells. The calcium ionophore, ionomycin, slightly enhanced the production of intracellular (icIL-1 α ), but this resulted in a necrotic release at higher concentrations. UV-B exposure significantly increased the production of icIL-1 α  in a dose-dependent manner with a maximal induction exhibited at 24 h with minimal necrotic and apoptotic effects. Validation of the HaCaT cell model indicated that the nonsteroidal anti-inflammatory drug (NSAID), ibuprofen, and the glucocorticoid, dexamethasone, inhibited icIL-1 α  production, and this was associated with a slight inhibition of cell viability. The UV-B-induced keratinocyte cell model provides an  in vitro  system that could, apart from phorbol ester-like compounds, be utilised as a screening assay in identifying skin irritants and/or therapeutic topical agents via the modulation of IL-1 α  production.

journal of skin cancer

Interleukin-1<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi mathvariant="bold">α</mml:mi></mml:math>Induction in Human Keratinocytes (HaCaT): An<i>In Vitro</i>Model for Chemoprevention in Skin

Interleukin-1αInduction in Human Keratinocytes (HaCaT): AnIn VitroModel for Chemoprevention in Skin