Macrophage Migration Inhibitory Factor Deficiency Causes Prolonged Hearing Loss After Acoustic Overstimulation

Shin Kariya1, Mitsuhiro Okano, Yukihide Maeda

  • 1*Department of Otolaryngology-Head and Neck Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama; and †Department of Medical Bioinformatics, Hokkaido Information University, Hokkaido, Japan.

Abstract

Insights

Macrophage migration inhibitory factor (MIF) deficiency prolonged hearing loss and hair cell damage after noise exposure. MIF may be crucial for recovering from acoustic trauma and offers a potential therapeutic target for noise-induced hearing loss.

Area of Science:

  • Ototolaryngology
  • Immunology
  • Cell Biology

Background:

  • Macrophage migration inhibitory factor (MIF) is vital for neural development and expressed in the inner ear.
  • Its specific role in auditory function, particularly in noise-induced hearing loss, is not well understood.

Purpose of the Study:

  • To investigate the role of MIF in noise-induced hearing loss and cochlear damage.
  • To determine if MIF deficiency exacerbates hearing impairment and hair cell loss following acoustic trauma.

Main Methods:

  • Utilized MIF-deficient (MIF(-/-)) and wild-type mice exposed to octave band noise.
  • Assessed auditory brainstem response thresholds, cochlear hair cell morphology via scanning electron microscopy, and cell apoptosis using TUNEL assay.

Main Results:

  • Both mouse groups experienced significant hearing loss post-noise exposure.
  • MIF(-/-) mice exhibited elevated hearing thresholds and greater outer hair cell damage 2 weeks after noise exposure compared to wild-type mice.
  • TUNEL-positive cells, indicating apoptosis, were observed in the organ of Corti of MIF(-/-) mice.

Conclusions:

  • MIF deficiency leads to prolonged hearing loss and cochlear hair cell loss after noise exposure.
  • MIF appears to play a significant role in the recovery process from acoustic trauma.
  • Modulating MIF levels could represent a novel therapeutic strategy for managing noise-induced hearing loss.

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