Establishing Transcription Profile of Psoriasiform Cutaneous In Vitro using HaCaT Cells Stimulated with Combination of Cytokines

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 participants in innate immunity,...

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Veröffentlicht in:Journal of visualized experiments 2021-03 (169)
Hauptverfasser: Zheng, Huaping, Gu, Linna, Wang, Zhen, Zhou, Hong, Zhang, Chen, Teng, Xiu, Hu, Zhonglan, Wei, Xiaoqiong, Liu, Xiao, Zeng, Fanlian, Zhao, Qixiang, Hao, Yan, Hu, Yawen, Wang, Xiaoyan, Hu, Jing, Yu, Jiadong, Wu, Wenlin, Zhou, Yifan, Cui, Kaijun, Huang, Nongyu, Li, Jiong
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Sprache:eng
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Zusammenfassung: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 participants 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 at transcription level with HaCaT cell line using five proinflammatory cytokines combination (M5 combination), including IL-17A, IL-22, IL-1α, TNF-α, and oncostatin M. Results demonstrate that M5 combination induced HaCaT cells showed increased levels of antimicrobial peptides (BD2, S100A7, S100A8, and S100A9), chemokines, and cytokines (CXCL1, CXCL2, CXCL8, CCL20, IL-1β, IL-6 and, IL-18). The mRNA levels of keratinocytes differentiation markers (Keratin1, Keratin10, Filaggrin, and Loricrin) were down regulated, which was consistent with the transcriptome data derived from psoriasis-like keratinocytes. The method described here, therefore, establishes an in vitro psoriasiform cutaneous inflammation at transcription level and contributes to the research for molecular pathogenesis of psoriasis.
ISSN:1940-087X
1940-087X
DOI:10.3791/61537