Yang Shurui, Chen Li, Zhang Haiming, Song Yanjuan, Wang Wenyan, Hu Zhengbo, Wang Siyu, Huang Liuyang, Wang Yayuan, Wu Song, Chen Rui, Liang Fengxia
College of Acupuncture and Orthopedics, Hubei University of Chinese Medicine, Wuhan, 430061, China.
Hubei Provincial Collaborative Innovation Center of Preventive Treatment by Acupuncture and Moxibustion, Wuhan, 430061, China.
J Neuroinflammation. 2025 Mar 11;22(1):75. doi: 10.1186/s12974-025-03397-4.
Chronic urticaria (CU) arises from a multifaceted interplay of immunological, neurological, and psychological components. Immune dysregulation, mediated through both immunoglobulin E (IgE)-dependent and IgE-independent pathways, plays a pivotal role in CU pathogenesis, involving key effector cells such as mast cells (MCs), basophils, and eosinophils. This dysregulation culminates in the release of histamine, prostaglandins, and other mediators, which precipitate pruritus. The chronicity of the disease leads to sustained pruritic symptoms, contributing to both central and peripheral sensitization. The excitation of the itch circuit is augmented, leading to the release of neurotransmitters and neuropeptides, which subsequently interact with immune cells. Psychological factors such as depression, anxiety, and stress exacerbate CU symptoms and diminish quality of life. These factors disrupt the hypothalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system (ANS). Furthermore, the act of scratching activates the reward circuit, resulting in the manifestation of the itch-scratching cycle. Current treatments, such as antihistamines, omalizumab, and cyclosporine, demonstrate variable efficacy and are often associated with adverse effects. A holistic approach addressing both psychological and physiological aspects is advocated. This review highlights the critical importance of understanding neuroimmune interactions and the influence of psychosomatic factors in CU. It aims to enhance diagnostic and therapeutic strategies by integrating psychological, neurological, and immunological perspectives.
慢性荨麻疹（CU）源于免疫、神经和心理成分的多方面相互作用。通过免疫球蛋白E（IgE）依赖性和非IgE依赖性途径介导的免疫失调在CU发病机制中起关键作用，涉及肥大细胞（MC）、嗜碱性粒细胞和嗜酸性粒细胞等关键效应细胞。这种失调最终导致组胺、前列腺素和其他介质的释放，从而引发瘙痒。疾病的慢性导致持续的瘙痒症状，促成中枢和外周致敏。瘙痒回路的兴奋增强，导致神经递质和神经肽的释放，随后与免疫细胞相互作用。抑郁、焦虑和压力等心理因素会加重CU症状并降低生活质量。这些因素会扰乱下丘脑-垂体-肾上腺（HPA）轴和自主神经系统（ANS）。此外，搔抓行为会激活奖赏回路，导致瘙痒-搔抓循环的出现。目前的治疗方法，如抗组胺药、奥马珠单抗和环孢素，疗效不一，且常伴有不良反应。提倡采用兼顾心理和生理方面的整体方法。本综述强调了理解神经免疫相互作用以及心身因素在CU中的影响的至关重要性。它旨在通过整合心理、神经和免疫观点来加强诊断和治疗策略。
