| Literature DB >> 33779603 |
Huaping Zheng1, Linna Gu1, Zhen Wang1, Hong Zhou1, Chen Zhang1, Xiu Teng1, Zhonglan Hu1, Xiaoqiong Wei1, Xiao Liu1, Fanlian Zeng1, Qixiang Zhao1, Yan Hao1, Yawen Hu1, Xiaoyan Wang1, Jing Hu1, Jiadong Yu1, Wenlin Wu1, Yifan Zhou1, Kaijun Cui2, Nongyu Huang1, Jiong Li3.
Abstract
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.Entities:
Year: 2021 PMID: 33779603 DOI: 10.3791/61537
Source DB: PubMed Journal: J Vis Exp ISSN: 1940-087X Impact factor: 1.355