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首页> 外文期刊>Archives of Toxicology >Keratinocyte-derived IL-36 gamma plays a role in hydroquinone-induced chemical leukoderma through inhibition of melanogenesis in human epidermal melanocytes
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Keratinocyte-derived IL-36 gamma plays a role in hydroquinone-induced chemical leukoderma through inhibition of melanogenesis in human epidermal melanocytes

机译：角质形成细胞衍生的IL-36γ在氢醌诱导的化学Leukoderma中发挥作用，通过抑制人体表皮黑色细胞中的素质生成

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摘要

Chemical leukoderma is an acquired type of vitiligo that can be initiated by various exogenous chemicals such as hydroquinone (HQ), rhododendrol (RD), or 4-tertiary butyl phenol (4-TBP). Despite the importance of epidermal keratinocytes in diverse dermatological conditions, their toxicological role in chemical leukoderma is poorly understood. To elucidate their role in the pathogenesis of chemical leukoderma, genome-scale transcriptional analysis was performed in human epidermal keratinocytes (HEKs) treated with a sub-cytotoxic HQ concentration (10 mu M). The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway-based functional enrichment analysis of HQ-induced differentially expressed genes (DEGs) revealed that HQ significantly upregulated DEGs related to the IL-17 signaling pathway and significantly downregulated DEGs associated with melanogenesis in HEKs. The meta-analysis between the HQ-induced and cytokine-induced transcriptional data (GSE53751) showed that 58 DEGs were commonly upregulated between HQ- and IL-17A-treated HEKs. Notably, the expression of IL36G was significantly increased in HEKs in response to both HQ and IL-17A. IL-36 gamma (2 mu g/ml) directly inhibits melanin biosynthesis in cultured human epidermal melanocytes (HEMs) and downregulates the gene transcription of key enzymes in the melanogenesis pathway including TYR, DCT, and TYRP1. Moreover, IL-36 gamma autocrinally regulated keratinocyte function to produce the proinflammatory cytokines IL-36 gamma, IL-6, and CXCL8/IL-8 in a concentration-dependent manner, suggesting that IL-36 gamma may stimulate the amplification cycle of cutaneous inflammation. In this regard, hydroquinone-induced IL-36 gamma from human keratinocytes plays a pivotal role in the development of chemical leukoderma by autocrinally or paracrinally modulating the crosstalk between keratinocytes and melanocytes.
机译：化学Leukoderma是一种获得的白癜风型，其可以通过各种外源化学品如氢醌（HQ），罗二甲醇（RD）或4-叔丁基苯酚（4-TBP）引发。尽管表皮角质形成细胞在不同的皮肤病中的重要性，但它们在化学Leukoderma中的毒理学作用很难理解。为了阐明其在化学白细胞病发病机制中的作用，在用亚细胞毒性HQ浓度（10μm）处理的人表皮角蛋白细胞（HEAK）中进行基因组级转录分析。基因和基因组（KEGG）基因组（KEGG）型差异的差异表达基因（DEGS）的京都常规富集分析表明，HQ与IL-17信号传导途径有关的次数显着上调，并显着下调与HEAK中的混合物相关的糖果。 HQ诱导和细胞因子诱导的转录数据（GSE53751）之间的META分析表明，在HQ-和IL-17A处理的HEK之间通常常见地上调58次。值得注意的是，响应于HQ和IL-17A，HEKES的表达明显增加。 IL-36γ（2μg/ ml）直接抑制培养的人表皮黑色细胞（HEMS）中的黑色素生物合成，下调素质生成途径中的关键酶的基因转录，包括Tyr，DCT和Tyrp1。此外，IL-36伽马自主基调的角质形成细胞肌细胞功能以浓度依赖性方式生产促炎细胞因子IL-36γ，IL-6和CXCL8 / IL-8，表明IL-36γ可以刺激皮肤的扩增循环炎。在这方面，来自人角蛋白细胞的氢醌诱导的IL-36γ在通过自认生或映射地调节角质形成细胞和黑色细胞之间的串扰来发挥化学白发霉菌的枢转作用。

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