ArticleHistochemistry and cell biology2016
Characterisation of cochlear inflammation in mice following acute and chronic noise exposure.
Article in Histochemistry and cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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Who cites it
97 citing papers in PubMed, 160 citations in OpenAlex.
- Inflammatory Signatures of Tinnitus in Patients and Mice.Neuroscience bulletin · 2026Article
- Navigating the Genetic Risk of Chemotherapy-Induced Hearing Loss in the Stria Vascularis.Clinical pharmacology and therapeutics · 2026Review
- Association between noise pollution perception and prevalence of cardiovascular disease in a Chinese adult population: a cross-sectional study based on the CGSS 2021 cardiovascular disease dataset.Frontiers in public health · 2026Article
- PLGA nanoparticles in otoprotection and inner ear regeneration: a new frontier in nanomedicine for hearing disorders.RSC advances · 2025Review
- Cochlear Homeostasis in Sensorineural Hearing Loss: Mechanisms, Implications, and Therapeutic Prospects.International journal of molecular sciences · 2025Review
- Targeting NLRP3/caspase-1/GSDMD to treat inner ear injury from labyrinthine hemorrhage.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Quinolylnitrone 23 Protects from Auditory Cell Oxidative Injury and Noise-Induced Hearing Loss.ACS pharmacology & translational science · 2025Article
- Noise-Induced Hearing Loss: Overview and Future Prospects for Research on Oxidative Stress.International journal of molecular sciences · 2025Review
- Chronic Inflammation and Hearing Loss: Key Biomarkers and Subgroup Differences by Gender and BMI in a National Cohort.Immunity, inflammation and disease · 2025Article
- Early control of cochlear viral load limits cochlear inflammation and prevents virus-induced sensorineural hearing loss.Journal of neuroinflammation · 2025Article
- LDHA-mediated glycolysis in stria vascularis endothelial cells regulates macrophages function through CX3CL1-CX3CR1 pathway in noise-induced oxidative stress.Cell death & disease · 2025Article
- Transcriptome sequencing reveals regulatory genes associated with neurogenic hearing loss.BMC medical genomics · 2025Article
- Can exercise regulate the relationship between noise pollution and the perception of physical and mental health among Chinese adults? An empirical study based on CGSS 2021.Frontiers in public health · 2025Article
- CXFrontiers in immunology · 2025Article
- Interplay between noise-induced sensorineural hearing loss and hypertension: pathophysiological mechanisms and therapeutic prospects.Frontiers in cellular neuroscience · 2025Review
- Research progress in modulating the auditory system by the cochlear circadian clock system in response to noise exposure.Frontiers in neuroscience · 2025Review
- Oxidative stress and inflammation combine to exacerbate cochlear damage and sensorineural hearing loss in C57BL/6 mice.Frontiers in neuroscience · 2025Article
- Auditory and Vestibular Involvement in Congenital Cytomegalovirus Infection.Pathogens (Basel, Switzerland) · 2024Review
- Article
- ABCC1 deficiency potentiated noise-induced hearing loss in mice by impairing cochlear antioxidant capacity.Redox biology · 2024Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress has been established as the key mechanism of the cochlear damage underlying noise-induced hearing loss, however, emerging evidence suggests that cochlear inflammation may also be a major contributor. This study aimed to improve our understanding of the cochlear inflammatory response associated with acute and chronic noise exposure. C57BL/6 mice were exposed to acute traumatic noise (100 dBSPL, 8-16 kHz for 24 h) and their cochleae collected at various intervals thereafter, up to 7 days. Using quantitative RT-PCR and immunohistochemistry, changes in expression levels of proinflammatory cytokines (TNF-α, IL-1β), chemokines (CCL2) and cell adhesion molecules (ICAM-1) were studied. All gene transcripts displayed similar dynamics of expression, with an early upregulation at 6 h post-exposure, followed by a second peak at 7 days. ICAM-1 immunoexpression increased significantly in the inferior region of the spiral ligament, peaking 24 h post-exposure. The early expression of proinflammatory mediators likely mediates the recruitment and extravasation of inflammatory cells into the noise-exposed cochlea. The occurrence of the latter expression peak is not clear, but it may be associated with reparative processes initiated in response to cochlear damage. Chronic exposure to moderate noise (90 dBSPL, 8-16 kHz, 2 h/day, up to 4 weeks) also elicited an inflammatory response, reaching a maximum after 2 weeks, suggesting that cochlear damage and hearing loss associated with chronic environmental noise exposure may be linked to inflammatory processes in the cochlea. This study thus provides further insight into the dynamics of the cochlear inflammatory response induced by exposure to acute and chronic noise.
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