Objective

Hidradenitis suppurativa (HS) is a chronic inflammatory disease with limited treatment options; therefore, the current study investigated the downstream signaling pathways that are differentially expressed in HS subjects and may drive disease pathogenesis.

Methods

The expression of 144 genes was evaluated in the skin of 16 healthy subjects and 34 subjects with mild to severe HS using QuantiGene Plex assay.

Results

One hundred and twenty-nine genes were significantly elevated in lesional HS skin as compared to the skin of healthy controls including pro-inflammatory cytokines (IL-1α, IL-6, TNF-α), IL-17-associated cytokines (IL-17A, IL-17F, IL-23A), the IL-10 family of cytokines (IL-10, IL-19, IL-20, IL-22, IL-24), and IFN family members (IFNA1, IFNB1, IFNG, IL-12B). This corresponded with increased expression of tyrosine kinases (JAK1, JAK3, BTK, SYK) and their downstream signaling partners (STAT1, STAT2, STAT3, STAT5A, STAT5B, STAT6).

Conclusion

These data illustrate the diverse immune activation in lesional HS skin and suggest that deeper interrogation of the disease heterogeneity may reveal unique opportunities for targeted therapies in designated subpopulations.

中文翻译：

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化脓性汗腺炎皮肤的转录组学分析表明多种炎症通路在疾病发病机制中的作用。

客观的

化脓性汗腺炎 (HS) 是一种治疗选择有限的慢性炎症性疾病；因此，目前的研究调查了在 HS 受试者中差异表达并可能驱动疾病发病机制的下游信号通路。

方法

使用 QuantiGene Plex 测定法评估了 16 名健康受试者和 34 名轻度至重度 HS 受试者的皮肤中 144 个基因的表达。

结果

与健康对照的皮肤相比，HS 损伤皮肤中有 129 个基因显着升高，包括促炎细胞因子（IL-1α、IL-6、TNF-α）、IL-17 相关细胞因子（IL- 17A、IL-17F、IL-23A）、IL-10 细胞因子家族（IL-10、IL-19、IL-20、IL-22、IL-24）和 IFN 家族成员（IFNA1、IFNB1、IFNG , IL-12B)。这与酪氨酸激酶（JAK1、JAK3、BTK、SYK）及其下游信号伙伴（STAT1、STAT2、STAT3、STAT5A、STAT5B、STAT6）的表达增加相对应。

结论

这些数据说明了损伤性 HS 皮肤中的多种免疫激活，并表明对疾病异质性的更深入询问可能会揭示在指定亚群中进行靶向治疗的独特机会。