4.1 Article

MCP-1 produced by keratinocytes is associated with leucocyte recruitment during elicitation of nickel-induced occupational allergic contact dermatitis

期刊

TOXICOLOGY AND INDUSTRIAL HEALTH
卷 34, 期 1, 页码 36-43

出版社

SAGE PUBLICATIONS INC
DOI: 10.1177/0748233717738633

关键词

Monocyte chemoattractant peptide-1; occupational allergic contact dermatitis; nickel; HaCaT keratinocyte; leucocyte migration

资金

  1. Science and Technology Planning Project of Zhuhai city, China [2014D0401990013]
  2. Natural Science Foundation of Guangdong Province, China [2014A030313028]

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To investigate the expression profile of monocyte chemoattractant peptide-1 (MCP-1) by keratinocytes after nickel exposure and to identify its role for leucocyte migration during nickel-induced occupational allergic contact dermatitis (OACD), 26 workers diagnosed with nickel-induced OACD were enrolled. Skin biopsies from the positive nickel-challenged sites at different time points were assessed by immunohistochemistry (IHC) for MCP-1, CD68, CD45RO, and in situ hybridization (ISH) for MCP-1, using chronic periumbilical dermititis as controls. The expressions of MCP-1 in HaCaT cell culture after nickel treatment were quantified by enzyme-linked immunosorbent assay. The results showed that at positive nickel-challenged sites, strong expressions of MCP-1, both messenger RNA (mRNA) and protein, were detected in the basal keratinocytes during the early phase (24-48 h after nickel application), paralleled by the recruitment of CD68(+) and CD45RO(+) cells to the skin compartments. The expressions of MCP-1 declined gradually in the late phase (72-96 h after nickel application). Treatment with nickel sulfate at noncytotoxic concentrations (0.01-100 mu M) induced a concentration-related elevation of MCP-1 expression by HaCaT cells compared to the untreated cells. The data indicated that a temporal expression pattern of MCP-1 produced by keratinocytes after nickel exposure was involved in the complex process of mononuclear cell infiltration during elicitation of nickel-induced OACD. Targeting MCP-1 might be a potential therapeutic strategy for OACD.

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