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

Author:

Mai Weihua1,Lu Dongqing2,Liu Xingwei3,Chen Ling4

Affiliation:

1. Department of Preventive Medicine, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong, China

2. Department of Dermatology, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong, China

3. Department of General Surgery, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong, China

4. Department of Medical Quality Control, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong, China

Abstract

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 µM) 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.

Publisher

SAGE Publications

Subject

Health, Toxicology and Mutagenesis,Public Health, Environmental and Occupational Health,Toxicology

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