SIRT3 knockout aggravates LPS-induced eustachian tube dysfunction
Shimin Zong1
Huimin Zhang1
Ting Li1
Xi Lian1
Wei Tang1
Tianyi Liu2
Wenting Yu1
Xuan Yu1
Hongjun Xiao1
1.Department of Otorhinolaryngology-Head and Neck Surgery,Union Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430022,China;Institute of Otorhinolaryngology-Head and Neck Surgery,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430022,China;Hubei Province Clinical Research Center for Deafness and Vertigo,Wuhan 430022,China2.Department of Otorhinolaryngology-Head and Neck Surgery,Renmin Hospital,Wuhan University,Wuhan 430060,China
摘要：Purpose:Acute otitis media caused by gram-negative bacteria is a common otological condition among pediatric patients.Eustachian tube dysfunction(ETD)plays a pivotal role in the delayed resolution of acute otitis media,whereas the precise contribution of SIRT3 in this mechanism remains uncertain.This study aims to reveal the involvement of SIRT3 in murine ETD induced by LPS.Results:Histological analysis showed no baseline differences in ET structure between WT and SIRT3 knockout(SIRT3-KO)mice.However,LPS exposure led to increased goblet cell proliferation and MUC5AC mucus secretion in both genotypes,with SIRT3-KO exacerbating these effects.The SIRT3-KO group displayed reduced cilia length.Functionally,SIRT3-KO mice showed a significantly higher initial POP and decreased MCC compared to the WT group after LPS exposure.Additionally,the active clearance of negative pressure(ACNP)was significantly reduced in SIRT3-KO mice,indicating compromised ET function.Conclusions:SIRT3-KO increased resistance to ET opening in mice exposed to LPS,and this effect may be related to the upregulated MUC5AC expression,the increased surface tension of the luminal fluid and the impaired MCC function in mice exposed to LPS.
机标关键词：knockoutsirt3aggravatesdysfunctioneustachianlps-inducedtube
论文发表日期：2025-10-30
在线出版日期：2025-11-27（本平台首次上网日期，不代表文献的发表时间）
页数：8( 211-218 )
英文信息