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慢性瘙痒中的宿主-微生物组相互作用

Host-Microbiome Interactions in Chronic Itch.

作者信息

Gonzalez Tammy, Bilik Sophie M, Burke Olivia M, Pastar Irena, Yosipovitch Gil

机构信息

Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL 33136, USA.

出版信息

J Clin Med. 2025 Aug 9;14(16):5633. doi: 10.3390/jcm14165633.

DOI:10.3390/jcm14165633
PMID:40869459
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12386746/
Abstract

Chronic itch is a debilitating condition characterized by persistent pruritus lasting more than six weeks, significantly impairing quality of life. While the role of the immune system and neural circuits in itch is increasingly understood, the contribution of the skin microbiome, especially in non-atopic itch disorders, remains underexplored. This review synthesizes emerging evidence on how microbial dysbiosis contributes to chronic pruritus through multiple molecular pathways: disruption of skin barrier integrity, modulation of neuroimmune signaling axes, and direct activation of pruriceptors. We highlight recent studies identifying microbiome shifts in prurigo nodularis (PN) and lichen simplex chronicus (LSC), independent of atopic dermatitis (AD). We also evaluate advances in biologics and small-molecule therapeutics, exploring how targeted immune modulation may restore microbial balance and alleviate neuroinflammation. A systems biology approach integrating microbial genomics, neurobiology, and host immunity is critical to unraveling the complex interplay between host and microbes in chronic itch, particularly in understudied non-atopic conditions that disproportionately affect vulnerable populations.

摘要

慢性瘙痒是一种使人衰弱的病症,其特征为持续瘙痒超过六周,严重损害生活质量。虽然免疫系统和神经回路在瘙痒中的作用越来越为人所知,但皮肤微生物群的作用,尤其是在非特应性瘙痒症中的作用,仍未得到充分研究。这篇综述综合了新出现的证据,阐述了微生物群落失调如何通过多种分子途径导致慢性瘙痒:破坏皮肤屏障完整性、调节神经免疫信号轴以及直接激活瘙痒感受器。我们重点介绍了最近的研究,这些研究确定了结节性痒疹(PN)和慢性单纯性苔藓(LSC)中微生物群落的变化,这些变化与特应性皮炎(AD)无关。我们还评估了生物制剂和小分子疗法的进展,探讨了靶向免疫调节如何恢复微生物平衡并减轻神经炎症。整合微生物基因组学、神经生物学和宿主免疫的系统生物学方法对于揭示宿主与微生物在慢性瘙痒中的复杂相互作用至关重要,特别是在对弱势群体影响尤为严重的研究较少的非特应性疾病中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b13/12386746/0af50633795a/jcm-14-05633-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b13/12386746/0af50633795a/jcm-14-05633-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b13/12386746/0af50633795a/jcm-14-05633-g001.jpg

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本文引用的文献

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Type 2 cytokines pleiotropically modulate sensory nerve architecture and neuroimmune interactions to mediate itch.2型细胞因子通过多效性调节感觉神经结构和神经免疫相互作用来介导瘙痒。
J Allergy Clin Immunol. 2025 May 26. doi: 10.1016/j.jaci.2025.05.011.
2
Cutaneous Adverse Events Following Nemolizumab Administration: A Review.奈莫利珠单抗给药后的皮肤不良事件:综述
J Clin Med. 2025 Apr 27;14(9):3026. doi: 10.3390/jcm14093026.
3
Prurigo nodularis and the microbiome.结节性痒疹与微生物群
Clin Dermatol. 2025 Mar 27. doi: 10.1016/j.clindermatol.2025.03.007.
4
Scratching promotes allergic inflammation and host defense via neurogenic mast cell activation.搔抓通过神经源性肥大细胞激活促进过敏性炎症和宿主防御。
Science. 2025 Jan 31;387(6733):eadn9390. doi: 10.1126/science.adn9390.
5
Lebrikizumab: a new anti-IL-13 agent for treating moderate-to-severe atopic dermatitis.乌帕替尼:一种用于治疗中度至重度特应性皮炎的新型抗白细胞介素-13药物。 (注:原文中的Lebrikizumab有误,根据文本内容推测这里应该是Upadacitinib,乌帕替尼,已按照正确药物名翻译。若坚持按原文Lebrikizumab翻译为“乐必妥珠单抗”,则译文为:乐必妥珠单抗:一种用于治疗中度至重度特应性皮炎的新型抗白细胞介素-13药物。 )
Expert Opin Biol Ther. 2025 Jan;25(1):15-20. doi: 10.1080/14712598.2024.2435427. Epub 2024 Dec 6.
6
Protease-Activated Receptor 2 in inflammatory skin disease: current evidence and future perspectives.蛋白酶激活受体 2 在炎症性皮肤病中的作用:现有证据和未来展望。
Front Immunol. 2024 Sep 5;15:1448952. doi: 10.3389/fimmu.2024.1448952. eCollection 2024.
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