Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2026
CSNK1A1 Mediates Inner Ear Inflammation and Endolymphatic Hydrops in a Lipopolysaccharide-Induced Mouse Model.
СтатьяНазвание и аннотация: Перевод в очереди
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Deng Wenting, Lai Lan, Li Zhuangzhuang, Ou Yongkang, Zheng Yiqing, Xiong Hao
Аннотация
OBJECTIVE: Our previous studies demonstrated that casein kinase 1α1 (CSNK1A1) was significantly upregulated in the endolymphatic sac of patients with Meniere's disease (MD). However, its specific role in the development of MD remains unclear. This study aims to investigate the effects of CSNK1A1 inhibition on alleviating hydrops, inflammation, and preserving audiovestibular function in a mouse model of endolymphatic hydrops (EH).
STUDY DESIGN: Experimental animal study.
SETTING: Translational research laboratory.
METHODS: An EH model was induced in mice by postauricular lipopolysaccharide (LPS) injection. CSNK1A1 localization in hair cells was visualized via immunofluorescence. To functionally interrogate CSNK1A1, mice received intraperitoneal injections of the CSNK1A1 inhibitor CSNK1-IN-2. Evaluations encompassed three key parameters: cochlear morphology (EH severity), auditory brainstem response (ABR) and vestibular evoked myogenic potential (VEMP, audiovestibular function), and immunofluorescence for CD45 and F4/80 (macrophage infiltration).
RESULTS: In LPS-induced EH mice, CSNK1A1 expression was significantly upregulated in cochlear and vestibular hair cells. Pharmacological inhibition of CSNK1A1 markedly improved audiovestibular function, reducing ABR thresholds (all frequencies, P < .01) and attenuating VEMP latency prolongations (P < .0001), CSNK1A1 inhibition also reduced EH, decreasing the membrane length increase rate (P < .01), and decreased the infiltration of CD45+ and F4/80+ inflammatory macrophages in the cochlea and vestibule (P < .05).
CONCLUSION: CSNK1A1 plays a role in attenuating LPS-induced inner ear injury, suggesting that its inhibition may represent a potential strategy for attenuating inflammation-associated cochleovestibular damage.
STUDY DESIGN: Experimental animal study.
SETTING: Translational research laboratory.
METHODS: An EH model was induced in mice by postauricular lipopolysaccharide (LPS) injection. CSNK1A1 localization in hair cells was visualized via immunofluorescence. To functionally interrogate CSNK1A1, mice received intraperitoneal injections of the CSNK1A1 inhibitor CSNK1-IN-2. Evaluations encompassed three key parameters: cochlear morphology (EH severity), auditory brainstem response (ABR) and vestibular evoked myogenic potential (VEMP, audiovestibular function), and immunofluorescence for CD45 and F4/80 (macrophage infiltration).
RESULTS: In LPS-induced EH mice, CSNK1A1 expression was significantly upregulated in cochlear and vestibular hair cells. Pharmacological inhibition of CSNK1A1 markedly improved audiovestibular function, reducing ABR thresholds (all frequencies, P < .01) and attenuating VEMP latency prolongations (P < .0001), CSNK1A1 inhibition also reduced EH, decreasing the membrane length increase rate (P < .01), and decreased the infiltration of CD45+ and F4/80+ inflammatory macrophages in the cochlea and vestibule (P < .05).
CONCLUSION: CSNK1A1 plays a role in attenuating LPS-induced inner ear injury, suggesting that its inhibition may represent a potential strategy for attenuating inflammation-associated cochleovestibular damage.