Establishing In Vitro Inflammatory Model of Psoriasiform Cutaneous Using HaCaT Cells Stimulated with Combination of Cytokines
Establishing In Vitro Inflammatory Model of Psoriasiform Cutaneous Using HaCaT Cells Stimulated with Combination of Cytokines
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细胞因子组合刺激HaCaT细胞建立银屑病皮肤体外炎症模型
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通讯作者：
Jiong Li
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作者：
Huaping Zheng;Linna GU;Hong Zhou;Zhen Wang;Jiong Li
银屑病是一种常见的由先天性和适应性免疫系统介导的慢性炎症性皮肤病，以表皮角质形成细胞的异常增殖和分化以及炎性细胞的浸润为特征。皮肤特异性角质形成细胞是先天免疫的关键参与者，对免疫细胞和环境刺激做出反应，从而在银屑病的免疫发病机制中发挥重要作用。本研究采用5种促炎细胞因子（IL-17 A、IL-22、IL-1α、TNF-α和抑瘤素M）联合（M5）诱导HaCaT细胞建立银屑病样角质形成细胞炎症模型。结果表明，M5联合诱导的HaCaT细胞系显示出明显的细胞毒作用。60..抗微生物肽（BD 2、S100 A7、S100 A8和S100 A9）、趋化因子的产生增加。61..和细胞因子（CXCL 1、CXCL 2、CXCL 8、CCL 20、IL-1β、IL-6和IL-18）。角质形成细胞的表达。62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82.分化标志物（角蛋白1，角蛋白10，聚丝蛋白和兜甲蛋白）下调，与银屑病样角质形成细胞的转录组数据一致。同时，银屑病皮损中GEO谱的表达模式与M5联合诱导的HaCaT体外模型一致。总之，本文所述的方法将有助于建立体外银屑病样皮肤炎症模型，并有助于银屑病分子发病机制的研究，并确定新的关键致病性皮肤特异性分子用于治疗银屑病。
Psoriasis is a common chronic inflammatory skin disease mediated by innate and adaptive immune systems, characterized by abnormal proliferation and differentiation of epidermal keratinocytes and infiltration of inflammatory cells. Skin-specific keratinocytes are key participant in innate immunity, responding to immune cells and environmental stimulation, thereby serving an important role in the immunopathogenesis of psoriasis. Here, we present a method for inducing psoriasiform keratinocytes inflammation model with HaCaT cell line using five proinflammatory cytokines combination (M5 combination), including IL-17A, IL-22, IL-1α, TNF-α and oncostatin M. Results showed that M5 combination induced HaCaT cell line showed..60..increased production of antimicrobial peptides (BD2, S100A7, S100A8 and S100A9), chemokines..61..and cytokines (CXCL1, CXCL2, CXCL8, CCL20, IL-1β, IL-6 and IL-18)...The expression of keratinocytes..62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82..differentiation markers (Keratin1, Keratin10, Filaggrin and Loricrin) were down-regulated, consistent with transcriptome data derived from psoriasis‑ like keratinocytes. Meanwhile, the expression pattern of GEO profile in psoriatic skin lesions was consistent with M5 combination induced HaCaT in vitro model. Together, the methods described here will be useful for establishing an in vitro psoriasiform cutaneous inflammatory model and contribute to the research for molecular pathogenesis of psoriasis and identify novel key pathogenic skin-specific molecules for treating psoriasis.