ArticleMolecular medicine (Cambridge, Mass.)2025
Inhibition of TLR4 mitigates sensorineural hearing loss resulting from cochlear inflammation.
Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Characterization of the Middle Ear Microbiome in Meniere's Disease by 16S rRNA Gene Sequencing Compared to Chronic Suppurative Otitis Media.World journal of otorhinolaryngology - head and neck surgery · 2026Article
- Subtype-Specific Vulnerability of Spiral Ganglion Neurons in Sensorineural Hearing Loss Across the Lifespan.Brain sciences · 2026Review
- Navigating the Genetic Risk of Chemotherapy-Induced Hearing Loss in the Stria Vascularis.Clinical pharmacology and therapeutics · 2026Review
- Effect of adding biologic agents to disease-modifying anti-rheumatic drugs for refractory chronic suppurative otitis media: comparative outcomes and cytokine-driven mechanisms.American journal of translational research · 2026Article
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Authors and funding
12 authors.
Funding
Abstract
backgroundInflammation is a principal cause of sensorineural hearing loss resulting from cochlear injury. However, current research investigating the mechanisms of sensorineural inflammatory injury remains inadequate.
methodsCochlear inflammation was induced by administering lipopolysaccharide (LPS) into the otic bulla (OB) and posterior semicircular canal (PSCC). Auditory brainstem responses (ABR) were recorded, and cochlear tissue alterations were analyzed using hematoxylin and eosin (HE) staining and immunofluorescence. Levels of cochlear inflammation were quantified using a cytokine array. Additionally, Toll-like receptor 4 (TLR4) knockout mice were employed to evaluate sensorineural neuroprotection.
resultsLPS injection into the PSCC caused more pronounced and stable cochlear inflammatory damage compared to injection into the OB. LPS exposure led to significant loss of cochlear hair cells, atrophy of the stria vascularis, and spiral ganglion damage. Furthermore, LPS treatment upregulated TLR4 receptor expression, increased the number of Ionized calcium-binding adapter molecule 1 (IBA1) positive cells, and elevated levels of inflammatory cytokines in the cochlea. TLR4 knockout (TLR4-KO) mice demonstrated reduced LPS-induced cochlear sensorineural damage.
conclusionLPS injection into the PSCC induces sensorineural tissue damage in the cochlea and results in sensorineural hearing loss. These findings suggest that TLR4 inhibition can alleviate cochlear inflammation-induced sensorineural hearing loss. TLR4 represents a potential therapeutic target for sensorineural hearing loss.
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