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Peer-reviewedCC BY-NC-ND 4.0International Journal of Molecular Medicine

Mechanisms of neuroimmune crosstalk in vestibular disorders: Linking inflammation with neural circuit dysfunction (Review)

  • Xianfang Pan1
  • Jin Fan1
  • Zhiyi Yang1
  • Zegang Yin1
  • Zhen Li1
  • Zhifeng Rui2
  • Hujun Zhang3
  • Yujie Li1
  • Hongjuan Zhang1
  1. 1Department of Neurology, General Hospital of Western Theater Command, Chengdu, Sichuan 610083, P.R. China
  2. 2Department of Diagnostic Ultrasound, General Hospital of Western Theater Command, Chengdu, Sichuan 610083, P.R. China
  3. 3Minimally Invasive Department, Lanzhou Time Laser Plastic and Aesthetic Hospital, Lanzhou, Gansu 730000, P.R. China
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Abstract

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.

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Cite

BibTeXRIS
BibTeX
@article{pan2026mechanisms,
  title = {{Mechanisms of neuroimmune crosstalk in vestibular disorders: Linking inflammation with neural circuit dysfunction (Review)}},
  author = {Xianfang Pan and Jin Fan and Zhiyi Yang and Zegang Yin and Zhen Li and Zhifeng Rui and Hujun Zhang and Yujie Li and Hongjuan Zhang},
  journal = {International Journal of Molecular Medicine},
  year = {2026},
  month = oct,
  doi = {10.3892/ijmm.2026.6009},
  url = {https://doi.org/10.3892/ijmm.2026.6009},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Mechanisms of neuroimmune crosstalk in vestibular disorders: Linking inflammation with neural circuit dysfunction (Review)
AU  - Xianfang Pan
AU  - Jin Fan
AU  - Zhiyi Yang
AU  - Zegang Yin
AU  - Zhen Li
AU  - Zhifeng Rui
AU  - Hujun Zhang
AU  - Yujie Li
AU  - Hongjuan Zhang
PY  - 2026
DA  - 2026/10/08
JO  - International Journal of Molecular Medicine
DO  - 10.3892/ijmm.2026.6009
UR  - https://doi.org/10.3892/ijmm.2026.6009
AB  - 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.
SN  - 1107-3756
SN  - 1791-244X
ER  -