过敏性皮炎（AD）是一种严重的炎症性皮肤疾病，其特点是增高的炎性细胞因子水平，为炎症的恶性循环提供燃料。虽然与AD相关的炎症重组人表皮（RHE）模型已建立，但对其全面的了解仍然有限。为了揭示变化并确定与AD相关的炎症中的潜在关键基因，我们构建了受到包括多聚核苷酸多聚胞苷酸酸（polyinosinic-polycytidylic acid，Poly(I:C)），肿瘤坏死因子α（TNF-α），白细胞介素4（IL-4）和白细胞介素13（IL-13）在内的炎症混合物刺激的RHE模型，并使用串联质谱标签-蛋白质组学和RNA-seq转录组学分析进行了检测。我们运用主成分分析（PCA）、基因本体论（Gene Ontology，GO）和基因与基因组百科全书（Kyoto Encyclopedia of Genes and Genomes，KEGG）通路功能富集进行相关基因和蛋白质的分析。蛋白质-蛋白质相互作用网络有助于鉴定关键基因，并通过qPCR和western blot进行了进一步确认。我们观察到在炎症RHE中高表达了胸腺基质淋巴样成分（thymic stromal lymphopoietin）。本研究鉴定到了2369个差异表达基因和880个差异表达蛋白质，在混合物诱导组与正常对照组之间。共有248个重叠的符号在各种生物过程和信号通路中富集，包括角化鳞状囊叶、细胞间连接、钙离子结合、细胞外基质受体、萜类骨架生物合成和过氧化物酶体增殖物激活受体信号通路等等。在这248个重叠的符号中，通过CytoHubba基于度数识别出了10个关键分子，即信号转导和转录激活子3（STAT3）、整合素亚基β1（ITGB1）、角质蛋白（FLG）、角质化鳞状花蛋白（IVL）、DEAD（Asp-Glu-Ala-Asp）盒多肽58（DDX58）、小富含脯氨酸蛋白1B（SPRR1B）、干扰素诱导的带螺旋C结构域1（IFIH1）、脱黏蛋白1（DSG1）、胶原蛋白XVIIα1链（COL17A1）和整合素亚基α6（ITGA6）。这些综合结果为AD的分子机制提供了有价值的见解，并提供了筛选用于AD治疗的化妆品配方的潜在工具。

Atopic dermatitis (AD) is a severe inflammatory skin disorder, characterized by elevated levels of proinflammatory cytokines that fuel a vicious cycle of inflammation. While inflammatory recombinant human epidermal (RHE) models relevant to AD have been established, comprehensive understanding remains limited. To illuminate changes and identify potential hub genes involved in AD-related inflammation, RHE models, stimulated by an inflammatory cocktail including polyinosinic-polycytidylic acid, tumor necrosis factor alpha (TNF-α), interleukin 4 (IL-4) and interleukin 13 (IL-13), were constructed and examined using tandem mass tags-proteomic coupled with RNA-seq transcriptomic analyses. Principal component analysis (PCA), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway functional enrichment were employed for the analysis of related genes and proteins. Protein-protein interaction networks helped identify hub genes, which were further confirmed by qPCR and western blot. We observed high expression of thymic stromal lymphopoietin in the inflammatory RHE. Our study identified 2369 differentially expressed genes and 880 differentially expressed proteins in the cocktail-induced group versus the normal control group. A total of 248 overlapping symbols were enriched in various biological processes and signaling pathways, including cornification envelope, cell-cell junction, calcium ion binding, extracellular matrix receptor, terpenoid backbone biosynthesis, and peroxisome proliferator-activated receptors signaling pathway, among others. Among the 248 overlapping symbols, CytoHubba identified 10 hub molecules, namely signal transducer and activator of transcription 3 (STAT3), integrin subunit beta 1 (ITGB1), filaggrin (FLG), involucrin (IVL), DEAD (Asp-Glu-Ala-Asp) box polypeptide 58 (DDX58), small proline rich protein 1B (SPRR1B), interferon induced with helicase C domain 1 (IFIH1), desmoglein 1 (DSG1), collagen type XVII alpha 1 chain (COL17A1), and integrin subunit alpha 6 (ITGA6), based on the degree. These integrated results offer valuable insights into the molecular mechanisms of AD and present potential tools for screening cosmetic formulations intended for the treatment of AD.