前庭疾病中神经免疫交互作用的机制：将炎症与神经回路功能障碍联系起来（综述）。
Mechanisms of neuroimmune crosstalk in vestibular disorders: Linking inflammation with neural circuit dysfunction (Review).
文献信息
| PMID | 42852636 |
|---|---|
| 原文 | 在 PubMed 查看原文 ↗ |
| 发表日期 | 2026 |
| 作者 | Xianfang Pan |
| 作者单位 | Department of Neurology, General Hospital of Western Theater Command, Chengdu, Sichuan 610083, P.R. China. |
| 期刊 | International journal of molecular medicine |
| SCI 分区 | Q1 |
| IF | 6.2 |
| 研究类型 | 综述 Meta · 基础／转化 |
| 所属专科 | 耳科 |
中文摘要
前庭疾病，如前庭性偏头痛（VM）和梅尼埃病（MD），涉及炎症与神经回路功能障碍之间复杂的相互作用。新出现的证据强调神经免疫交互作用是一个统一的病理生理框架。本综述综合了关于炎症细胞因子网络；包括降钙素基因相关肽和组胺在内的神经肽信号传导；胶质细胞反应；以及包括肠-前庭轴在内的全身免疫影响的最新知识。新出现的证据提示，可能不同的免疫学特征可区分VM与MD。说明性例子包括MD中IL-1β和巨噬细胞衍生的C-X-C基序趋化因子配体（CXCL）8升高，而通过PI3K/AKT信号通路起作用的CXCL10已被牵涉到VM的发病机制中。然而，直接比较研究仍然有限，且细胞因子研究之间的发现显示出一定的异质性。这些观察结果支持基于机制的亚型划分这一概念，作为一个有前景但需要进一步验证的框架。神经炎症对前庭代偿具有双重作用，适当校准的反应促进恢复，而过度或受抑制的炎症则损害可塑性。本综述整合了分子、细胞和全身神经免疫机制，提供了一个将炎症与前庭神经回路功能障碍联系起来的连贯框架。本研究的目的是为前庭疾病的未来生物标志物开发和精准治疗策略提供信息。
英文摘要
Vestibular disorders such as vestibular migraine (VM) and Menière's disease (MD) involve complex interactions between inflammation and neural circuit dysfunction. Emerging evidence highlights neuroimmune crosstalk as a unifying pathophysiological framework. The present review synthesized current knowledge on inflammatory cytokine networks; neuropeptide signaling including calcitonin gene‑related peptide and histamine; glial responses; and systemic immune influences including the gut‑vestibular axis. Emerging evidence suggests potentially distinct immunological profiles may differentiate VM from MD. Illustrative examples include elevated IL‑1β and macrophage‑derived C‑X‑C motif chemokine ligand (CXCL)8 in MD, whereas CXCL10 acting through the PI3K/AKT signaling pathway has been implicated in VM pathogenesis. However, direct comparative studies remain limited and findings across cytokine studies show some heterogeneity. These observations support the concept of mechanism‑based subtyping as a promising framework requiring further validation. Neuroinflammation has dual effects on vestibular compensation, with appropriately calibrated responses promoting recovery and excessive or suppressed inflammation impairing plasticity. The present review integrates molecular, cellular and systemic neuroimmune mechanisms to provide a cohesive framework linking inflammation with vestibular neural circuit dysfunction. The purpose of the present study was to inform future biomarker development and precision therapeutic strategies for vestibular disorders.