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Long-term Silencing of Intersectin-1s in Mouse Lungs by Repeated Delivery of a Specific siRNA via Cationic Liposomes. Evaluation of Knockdown Effects by Electron Microscopy
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SIRT3 knockout aggravates LPS-induced eustachian tube dysfunction.

Shimin Zong1,2,3, Huimin Zhang1,2,3, Ting Li1,2,3

  • 1Department of Otorhinolaryngology-Head and Neck Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

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PubMed
Summary
This summary is machine-generated.

Mice lacking SIRT3 show worsened Eustachian tube dysfunction (ETD) after LPS exposure, indicating SIRT3 is crucial for maintaining ET function and may be a therapeutic target for otitis media.

Keywords:
LPSMUC5ACSirt3eustachian tube dysfunction

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Area of Science:

  • Otolaryngology
  • Molecular Biology
  • Immunology

Background:

  • Acute otitis media (AOM) is common in children, often caused by gram-negative bacteria.
  • Eustachian tube dysfunction (ETD) delays AOM resolution, but the role of SIRT3 in this process is unclear.

Purpose of the Study:

  • To investigate the role of SIRT3 in LPS-induced murine ETD.

Main Methods:

  • Comparison of wild-type (WT) and SIRT3 knockout (SIRT3-KO) mice.
  • Histological analysis of Eustachian tube (ET) structure.
  • Assessment of goblet cell proliferation, MUC5AC secretion, cilia length, initial opening pressure (POP), mucociliary clearance (MCC), and active clearance of negative pressure (ACNP) after LPS exposure.

Main Results:

  • SIRT3-KO mice exhibited exacerbated LPS-induced goblet cell proliferation and MUC5AC secretion.
  • SIRT3-KO mice showed reduced cilia length, increased POP, decreased MCC, and impaired ACNP.
  • SIRT3 deficiency increased resistance to ET opening post-LPS exposure.

Conclusions:

  • SIRT3 deficiency worsens ETD in response to LPS.
  • Upregulated MUC5AC, increased luminal fluid surface tension, and impaired MCC function contribute to the exacerbated ETD in SIRT3-KO mice.