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Integrated Proteomic Profiling of Inner Ear and Systemic Fluids Following Noise-Induced Hearing Loss in Rats

ABSTRACT: This project investigates proteomic changes associated with noise-induced hearing loss (NIHL) using a rat model. Sprague–Dawley rats were exposed to acute broadband noise (110 dB SPL for 1 hour), resulting in an approximately 40 dB auditory threshold shift measured by cochlear nerve compound action potential (CAP). Proteomic profiling was performed on perilymph, cochlear-sourced cerebrospinal fluid (CSF), whole blood, and plasma to identify molecular responses to acoustic trauma. Comparative analysis revealed significant protein alterations across local cochlear fluids and systemic samples, highlighting pathways related to metabolism, immune responses, complement/coagulation, and lipid regulation. The dataset provides a resource for exploring molecular mechanisms of NIHL and identifying potential systemic biomarkers associated with cochlear injury.

ORGANISM(S): Rattus Rattus (black Rat)

SUBMITTER: Paul A. Haynes

PROVIDER: PXD075720 | JPOST Repository | Fri Mar 20 00:00:00 GMT 2026

REPOSITORIES: jPOST

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Project description:Background. COVID-19-induced neurological disease is a growing concern. Here we provide a comprehensive clinical, molecular, and neuroimaging investigation of patients presenting neurological symptoms to investigate underlying processes. Methods. We performed a detailed systematized clinical, laboratory, and neuroimaging (CT/MRI) data analysis from 35 mild to severe Brazilian COVID-19 hospitalised patients with clinical indications for cerebrospinal fluid (CSF) exam. In patients' CSF, we measured interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α) and the Alzheimer's disease-associated biomarkers amyloid-beta (Aβ)1-40, Aβ1-42, Tau and pTau181 levels (n=31-35). In addition, CSF proteomics and the search for SARS-CoV-2 spike protein presence using shotgun and targeted multiple reaction monitoring liquid-chromatography/mass-spectrometry were performed (n=16). We further evaluated a 29-cytokine panel in patients’ blood (n=16). An electronic questionnaire was conducted one-year post-hospitalisation (n=19, 63.3%). Findings. COVID-19 patients presented heterogeneous clinical and neurological features, including encephalopathy, encephalitis, and neuromuscular syndromes, despite low pulmonary burden. Patients showed increased circulating cytokines and CSF IL-6 and TNF-α levels compared to controls. Alzheimer’s disease-related biomarkers were unaltered compared to controls. COVID-19 altered CSF proteomic pathways associated to complement and coagulation cascades, immune-inflammatory, metabolism and amyloidosis. We found no traces of spike protein in patients’ CSF. Severe patients presented more pronounced neuroimaging alterations, altered CSF levels of IL-6, Tau, and Aβ-species compared to mild patients. Peripheral inflammation markers correlated with CSF IL-6 and Tau-species levels. Finally, in a one-year post-COVID survey, survivors were not recovered entirely (12/19) and reported confusion or memory/attention deficits (13/19). Interpretation. COVID-19 induces a broad spectrum of neurological presentations associated with changes in central nervous system (CNS) inflammatory and neurodegenerative molecular and structural biomarkers that correlate with systemic inflammation and disease severity. Given that neurological symptoms persist up to one-year post-COVID, our results urge us to investigate whether systemic, and CNS molecular changes are permanent or alleviated so that COVID-19 patients with lingering symptoms are adequately treated.

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Dataset Information

Integrated Proteomic Profiling of Inner Ear and Systemic Fluids Following Noise-Induced Hearing Loss in Rats

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