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Updated: Feb 8, 2026

Neuro-rehabilitation Approach for Sudden Sensorineural Hearing Loss
Published on: January 25, 2016
Inflammasome activation in mouse inner ear in response to MCMV induced hearing loss
Xi Shi1,2, Yanfen Dong1, Ya Li1
1The Institute of Audiology and Speech Science of Xuzhou Medical Collage, Xuzhou 221004, China.
Objective:
To identify presence of inflammasome activated in mouse cochlea with sensorineural hearing loss (SNHL) caused by cytomegalovirus (CMV) infection.
Method:
MCMV was injected into the right cerebral hemisphere in neonatal BALB/c mice at 2000 pfu virus titers. Auditory brainstem responses (ABRs) were tested to evaluate hearing at 21 days. Histopathological studies were conducted to confirm localizations of MCMV infected cells in the inner ear. Expression of inflammasome related factors was assessed by immunofluorescence, Quantitative real-time PCR and Western blotting.
Results:
In the mouse model of CMV induced SNHL, inflammasome related kinase Caspase-1 and downstream inflammatory factor IL-1β and IL-18 were found increased and activated after CMV infection in the cochlea. These factors could further up-regulate expression of IL-6 and TNF-α. These inflammatory factors are neurotoxicity and may contribute to hearing impairment. Furthermore, we also detected significantly increased AIM2 protein that accumulated in the SGN of cochleae with CMV infection.
Significance:
We have shown that inflammasome as a novel inherent immunity mechanism may contribute to hearing impairment.
Conclusion:
Our data indicate that imflammasome assemble in mouse inner ear in response to CMV infection. We have revealed a novel pathology event in CMV induced SNHL involving activation of inflammasome in mouse cochlea. Additionally, we have shown that inflammasome may be a novel target for prevention and treatment of CMV related SNHL.
Insights
Cytomegalovirus (CMV) infection activates the inflammasome in the mouse cochlea, contributing to sensorineural hearing loss (SNHL). This inflammasome activation presents a potential therapeutic target for CMV-related SNHL.
Area of Science:
- Immunology
- Otolaryngology
- Virology
Background:
- Cytomegalovirus (CMV) infection is a known cause of sensorineural hearing loss (SNHL).
- The role of the inflammasome, a key component of innate immunity, in CMV-induced SNHL is not well understood.
Purpose of the Study:
- To investigate the presence and activation of the inflammasome in the mouse cochlea following CMV infection.
- To explore the potential contribution of inflammasome activation to hearing impairment in a CMV-induced SNHL model.
Main Methods:
- A mouse model of CMV-induced SNHL was established using murine cytomegalovirus (MCMV).
- Hearing function was assessed using auditory brainstem responses (ABRs).
- Inflammasome components (Caspase-1, IL-1β, IL-18, AIM2) and inflammatory cytokines (IL-6, TNF-α) were quantified using immunofluorescence, qPCR, and Western blotting.
Main Results:
- CMV infection led to increased activation of Caspase-1 and downstream factors IL-1β and IL-18 in the cochlea.
- These inflammasome-related factors upregulated IL-6 and TNF-α expression, suggesting a neurotoxic inflammatory cascade.
- Elevated AIM2 protein levels were detected in the spiral ganglion neurons (SGN) of infected cochleae.
Conclusions:
- The inflammasome is activated in the mouse inner ear in response to CMV infection.
- Inflammasome activation represents a novel pathological mechanism in CMV-induced SNHL.
- Targeting the inflammasome may offer a new therapeutic strategy for preventing and treating CMV-related hearing loss.
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