PDF(Pubmed)
Abstract：
UNASSIGNED: Acne inversa (AI) is a refractory inflammatory skin disease, and TNF-α plays an important role in the pathogenesis of AI. By blocking TNF-α, infliximab (IFX) has been proven to be a promising method.
UNASSIGNED: To explore the underlying mechanisms of IFX treatment in AI patients.
UNASSIGNED: In this research, we integrated transcriptome sequencing data from the samples of our patients with AI and the GEO database. Ex vivo skin culture of AI patients was conducted to evaluate the efficacy of IFX treatment. Animal studies and cell experiments were used to explore the therapeutic effect and mechanism of IFX treatment.
UNASSIGNED: Both TNF-α and NLRP3 inflammasome-related pathways were enriched in skin lesions of AI patients and murine AI models. After IFX treatment, the NLRP3 inflammasome-related pathway was effectively blocked, and the IL-1β level was normalized in ex vivo AI skin explants and murine AI models. Mechanistically, IFX suppressed the NF-κB signaling pathway to lower the expression of NLRP3 and IL-1β in keratinocytes.
UNASSIGNED: IFX treatment alleviated skin lesions in murine AI models and downregulated NLRP3 and IL-1β expression levels by inhibiting the NF-κB signaling pathway, which was helpful for understanding the mechanism of IFX therapy.
UNASSIGNED: To explore the underlying mechanisms of IFX treatment in AI patients.
UNASSIGNED: In this research, we integrated transcriptome sequencing data from the samples of our patients with AI and the GEO database. Ex vivo skin culture of AI patients was conducted to evaluate the efficacy of IFX treatment. Animal studies and cell experiments were used to explore the therapeutic effect and mechanism of IFX treatment.
UNASSIGNED: Both TNF-α and NLRP3 inflammasome-related pathways were enriched in skin lesions of AI patients and murine AI models. After IFX treatment, the NLRP3 inflammasome-related pathway was effectively blocked, and the IL-1β level was normalized in ex vivo AI skin explants and murine AI models. Mechanistically, IFX suppressed the NF-κB signaling pathway to lower the expression of NLRP3 and IL-1β in keratinocytes.
UNASSIGNED: IFX treatment alleviated skin lesions in murine AI models and downregulated NLRP3 and IL-1β expression levels by inhibiting the NF-κB signaling pathway, which was helpful for understanding the mechanism of IFX therapy.
摘要：
■痤疮（AI）是一种难治性炎症性皮肤病，TNF-α在AI的发病机制中起重要作用。通过阻断TNF-α,英夫利昔单抗（IFX）已被证明是一种有前途的方法。
■探讨IFX治疗AI患者的潜在机制。
■在这项研究中，我们整合了AI患者样本和GEO数据库的转录组测序数据.进行AI患者的离体皮肤培养以评估IFX治疗的功效。通过动物实验和细胞实验探讨IFX治疗的疗效和作用机制。
■TNF-α和NLRP3炎性体相关通路在AI患者和小鼠AI模型的皮肤病变中均富集。IFX治疗后，NLRP3炎性体相关通路被有效阻断，IL-1β水平在离体AI皮肤外植体和小鼠AI模型中正常化。机械上,IFX抑制NF-κB信号通路以降低角质形成细胞中NLRP3和IL-1β的表达。
■IFX治疗通过抑制NF-κB信号通路减轻小鼠AI模型的皮肤损伤，下调NLRP3和IL-1β表达水平，这有助于理解IFX治疗的机制。
■探讨IFX治疗AI患者的潜在机制。
■在这项研究中，我们整合了AI患者样本和GEO数据库的转录组测序数据.进行AI患者的离体皮肤培养以评估IFX治疗的功效。通过动物实验和细胞实验探讨IFX治疗的疗效和作用机制。
■TNF-α和NLRP3炎性体相关通路在AI患者和小鼠AI模型的皮肤病变中均富集。IFX治疗后，NLRP3炎性体相关通路被有效阻断，IL-1β水平在离体AI皮肤外植体和小鼠AI模型中正常化。机械上,IFX抑制NF-κB信号通路以降低角质形成细胞中NLRP3和IL-1β的表达。
■IFX治疗通过抑制NF-κB信号通路减轻小鼠AI模型的皮肤损伤，下调NLRP3和IL-1β表达水平，这有助于理解IFX治疗的机制。
