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Biochem Biophys Res Commun. 2017 Nov 18;493(2):894-900. doi: 10.1016/j.bbrc.2017.09.124. Epub 2017 Sep 23.

Macrophage recruitment, but not interleukin 1 beta activation, enhances noise-induced hearing damage.

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Department of Otolaryngology and Head and Neck Surgery, Faculty of Medicine, University of Tokyo, Japan.
Department of Otolaryngology and Head and Neck Surgery, Faculty of Medicine, University of Tokyo, Japan. Electronic address:


It has been suggested that macrophages or inflammatory monocytes participate in the pathology of noise-induced hearing loss (NIHL), but it is unclear how extensively these cells contribute to the development of temporary and/or permanent NIHL. To address this question, we used clodronate liposomes to deplete macrophages and monocytes. After clodronate liposome injection, mice were exposed to 4-kHz octave band noise at 121 dB for 4 h. Compared to vehicle-injected controls, clodronate-treated mice exhibited significantly reduced permanent threshold shifts at 4 and 8 kHz and significantly smaller outer hair cell losses in the lower-apical cochlear turn. Following noise exposure, the stria vascularis had significantly more cells expressing the macrophage-specific protein F4/80, and this effect was significantly suppressed by clodronate treatment. These F4/80-positive cells expressed interleukin 1 beta (IL-1β), which noise exposure activated. However, IL-1β deficient mice did not exhibit significant resistance to intense noise when compared to wild-type mice. These findings suggest that macrophages that enter the cochlea after noise exposure are involved in NIHL, whereas IL-1β inhibition does not reverse this cochlear damage. Therefore, macrophages may be a promising therapeutic target in human sensorineural hearing losses such as NIHL.


Clodronate liposomes; F4/80; Interleukin 1 beta; Macrophages; Noise-induced hearing loss; Permanent threshold shift

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