A mouse model of autoimmune inner ear disease without endolymphatic hydrops.

Autoimmune inner ear disease Hearing loss Rheumatoid arthritis Type II collagen Vertigo

Journal

Biochimica et biophysica acta. Molecular basis of disease
ISSN: 1879-260X
Titre abrégé: Biochim Biophys Acta Mol Basis Dis
Pays: Netherlands
ID NLM: 101731730

Informations de publication

Date de publication:
24 Apr 2024
Historique:
received: 14 07 2023
revised: 25 03 2024
accepted: 17 04 2024
medline: 27 4 2024
pubmed: 27 4 2024
entrez: 26 4 2024
Statut: aheadofprint

Résumé

Autoimmune inner ear disease (AIED) is an organ-specific disease characterized by irreversible, prolonged, and progressive hearing and equilibrium dysfunctions. The primary symptoms of AIED include asymmetric sensorineural hearing loss accompanied by vertigo, aural fullness, and tinnitus. AIED is divided into primary and secondary types. Research has been conducted using animal models of rheumatoid arthritis (RA), a cause of secondary AIED. However, current models are insufficient to accurately analyze vestibular function, and the mechanism underlying the onset of AIED has not yet been fully elucidated. Elucidation of the mechanism of AIED onset is urgently needed to develop effective treatments. In the present study, we analyzed the pathogenesis of vertigo in autoimmune diseases using a mouse model of type II collagen-induced RA. Auditory brain stem response analysis demonstrated that the RA mouse models exhibited hearing loss, which is the primary symptom of AIED. In addition, our vestibulo-oculomotor reflex analysis, which is an excellent vestibular function test, accurately captured vertigo symptoms in the RA mouse models. Moreover, our results revealed that the cause of hearing loss and vestibular dysfunction was not endolymphatic hydrops, but rather structural destruction of the organ of Corti and the lateral semicircular canal ampulla due to an autoimmune reaction against type II collagen. Overall, we were able to establish a mouse model of AIED without endolymphatic hydrops. Our findings will help elucidate the mechanisms of hearing loss and vertigo associated with AIED and facilitate the development of new therapeutic methods.

Identifiants

pubmed: 38670439
pii: S0925-4439(24)00187-X
doi: 10.1016/j.bbadis.2024.167198
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

167198

Informations de copyright

Copyright © 2024. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Shotaro Harada (S)

Department of Neuroscience and Cell Biology, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan; Department of Otorhinolaryngology-Head and Neck Surgery, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.

Yoshihisa Koyama (Y)

Department of Neuroscience and Cell Biology, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan; Addiction Research Unit, Osaka Psychiatric Research Center, Osaka Psychiatric Medical Center, Osaka 541-8567, Japan; Global Center for Medical Engineering and Informatics, Osaka University, Suita 565-0871, Japan; Integrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives (OTRI), Osaka University, Suita 565-0871, Japan. Electronic address: koyama@anat2.med.osaka-u.ac.jp.

Takao Imai (T)

Department of Otorhinolaryngology-Head and Neck Surgery, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.

Yoshichika Yoshioka (Y)

Graduate School of Frontier Biosciences, Osaka University, Osaka 565-0871, Japan; Center for Information and Neural Networks, National Institute of Information and Communications Technology (NICT) and Osaka University, Osaka 565-0871, Japan; Institute for Open and Transdisciplinary Research Initiatives, Osaka University, Osaka 565-0871, Japan.

Takuya Sumi (T)

Department of Cell Biology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.

Hidenori Inohara (H)

Department of Otorhinolaryngology-Head and Neck Surgery, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.

Shoichi Shimada (S)

Department of Neuroscience and Cell Biology, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan; Addiction Research Unit, Osaka Psychiatric Research Center, Osaka Psychiatric Medical Center, Osaka 541-8567, Japan; Global Center for Medical Engineering and Informatics, Osaka University, Suita 565-0871, Japan.

Classifications MeSH