Abstract

Serological biomarkers of inner ear proteins are a promising new approach for studying human hearing. Here, we focus on the serological measurement of prestin, a protein integral to a human’s highly sensitive hearing, expressed in cochlear outer hair cells (OHCs). Building from recent nonhuman studies that associated noise-induced OHC trauma with reduced serum prestin levels, and studies suggesting subclinical hearing damage in humans regularly engaging in noisy activities, we investigated the relation between serum prestin levels and environmental noise levels in young adults with normal clinical audiograms. We measured prestin protein levels from circulating blood and collected noise level data multiple times over the course of the experiment using body-worn sound recorders. Results indicate that serum prestin levels have a negative relation with noise exposure: individuals with higher routine noise exposure levels tended to have lower prestin levels. Moreover, when grouping participants based on their risk for a clinically-significant noise-induced hearing loss, we found that prestin levels differed significantly between groups, even though behavioral hearing thresholds were similar. We discuss possible interpretations for our findings including whether lower serum levels may reflect subclinical levels of OHC damage, or possibly an adaptive, protective mechanism in which prestin expression is downregulated in response to loud environments.

Highlights

  • Venipuncture components of OHCs are released into the blood stream after the phagocytosis of damaged ­OHCs12–14

  • Because weak otoacoustic emissions (OAEs) can sometimes be an indicator of small levels of OHC ­loss[22,23], the relation between lower serum levels and weaker OAEs may suggest that serum prestin is sensitive to levels of OHC loss/damage too small to be detectable on the clinical audiogram

  • If prestin levels are driven by subclinical OHC loss from noise exposure, serum levels are expected to correlate with other metrics of subclinical hearing loss, such as extended high frequency (EHF) a­ udiometry[30,31,32]

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Summary

Introduction

Venipuncture components of OHCs are released into the blood stream after the phagocytosis of damaged ­OHCs12–14. Our findings indicated a significant albeit weak relation to otoacoustic emissions (OAEs) (transiently evoked OAEs—TEOAEs), a clinical test used for ototoxic monitoring and newborn hearing screenings that is currently considered the most direct clinical measure of OHC ­function[21] These earlier findings suggested that the broad range of circulating levels of prestin observed in this dataset could reflect individual differences in OHC function. Noise exposure (see Refs.[28,29] for studies examining subclinical cochlear damage in noise exposed populations), serum prestin levels are expected to decrease with increasing levels of noise exposure With this hypothesis, we would expect a negative relation between the two metrics, even in the absence of a clinically significant hearing loss as measured by an audiogram (“Hidden Outer Hair Cell Damage Hypothesis”). If prestin levels are driven by subclinical OHC loss from noise exposure, serum levels are expected to correlate with other metrics of subclinical hearing loss, such as extended high frequency (EHF) a­ udiometry[30,31,32]

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