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Peer-reviewedCC BYCell death discovery

CXCR2 deficiency impairs auditory function in spiral ganglion neurons by altering excitability.

  • Fuyu Xian1
  • Xueya Ma1
  • Zhongyang Zhang1
  • Cailin He1
  • Zeyuan Li1
  • Jiaxi Liu1
  • Xishuo Jin1
  • Jundan Xiao1
  • Haitao Shen2
  • Ping Lv3
  1. 1Department of Pharmacology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of New Drug Pharmacology and Toxicology, The Hebei Collaboration Innovation Center for Mechanism, Diagnosis and Treatment of Neurological and Psychiatric Disease, Hebei Medical University, Shijiazhuang, China.
  2. 2Lab of Pathology, Hebei Medical University, Shijiazhuang, China. [email protected].
  3. 3Department of Pharmacology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of New Drug Pharmacology and Toxicology, The Hebei Collaboration Innovation Center for Mechanism, Diagnosis and Treatment of Neurological and Psychiatric Disease, Hebei Medical University, Shijiazhuang, China. [email protected].
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Abstract

CXC chemokine receptor 2 (CXCR2), a key member of the chemokine receptor family, plays a central role in regulating immune and inflammatory responses. Inflammation has been established as a critical pathological factor in various auditory disorders, including noise-induced hearing loss, drug-induced ototoxicity, and age-related hearing loss; however, the expression patterns and biological functions of CXCR2 in key cells involved in auditory signal transduction remain unclear. Here, we demonstrated that CXCR2 is abundantly expressed in cochlear spiral ganglion neurons (SGNs), hair cells, and the stria vascularis. Genetic deletion of CXCR2 resulted in progressive hearing loss in mice. SGNs from CXCR2 knockout mice exhibited increased expression of the Kv1.2 potassium channel, impaired ribbon synapses, and altered myelin integrity. Electrophysiological analysis revealed enhanced Kv1 currents and significantly reduced excitability in CXCR2-deficient SGNs. Notably, CXCR2 knockdown in SGNs using an adeno-associated virus recapitulated the hearing loss phenotype. In conclusion, our findings revealed that CXCR2 is essential for hearing as it regulates SGN excitability.

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Cite

BibTeXRIS
BibTeX
@article{xian2026cxcr2,
  title = {{CXCR2 deficiency impairs auditory function in spiral ganglion neurons by altering excitability.}},
  author = {Fuyu Xian and Xueya Ma and Zhongyang Zhang and Cailin He and Zeyuan Li and Jiaxi Liu and Xishuo Jin and Jundan Xiao and Haitao Shen and Ping Lv},
  journal = {Cell death discovery},
  year = {2026},
  month = oct,
  doi = {10.1038/s41420-026-03366-7},
  url = {https://europepmc.org/article/MED/42957635},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - CXCR2 deficiency impairs auditory function in spiral ganglion neurons by altering excitability.
AU  - Fuyu Xian
AU  - Xueya Ma
AU  - Zhongyang Zhang
AU  - Cailin He
AU  - Zeyuan Li
AU  - Jiaxi Liu
AU  - Xishuo Jin
AU  - Jundan Xiao
AU  - Haitao Shen
AU  - Ping Lv
PY  - 2026
DA  - 2026/10/15
JO  - Cell death discovery
DO  - 10.1038/s41420-026-03366-7
UR  - https://europepmc.org/article/MED/42957635
AB  - CXC chemokine receptor 2 (CXCR2), a key member of the chemokine receptor family, plays a central role in regulating immune and inflammatory responses. Inflammation has been established as a critical pathological factor in various auditory disorders, including noise-induced hearing loss, drug-induced ototoxicity, and age-related hearing loss; however, the expression patterns and biological functions of CXCR2 in key cells involved in auditory signal transduction remain unclear. Here, we demonstrated that CXCR2 is abundantly expressed in cochlear spiral ganglion neurons (SGNs), hair cells, and the stria vascularis. Genetic deletion of CXCR2 resulted in progressive hearing loss in mice. SGNs from CXCR2 knockout mice exhibited increased expression of the Kv1.2 potassium channel, impaired ribbon synapses, and altered myelin integrity. Electrophysiological analysis revealed enhanced Kv1 currents and significantly reduced excitability in CXCR2-deficient SGNs. Notably, CXCR2 knockdown in SGNs using an adeno-associated virus recapitulated the hearing loss phenotype. In conclusion, our findings revealed that CXCR2 is essential for hearing as it regulates SGN excitability.
SN  - 2058-7716
ER  -