| First Author | Mizushima Y | Year | 2017 |
| Journal | Biochem Biophys Res Commun | Volume | 493 |
| Issue | 2 | Pages | 894-900 |
| PubMed ID | 28951212 | Mgi Jnum | J:251238 |
| Mgi Id | MGI:6102991 | Doi | 10.1016/j.bbrc.2017.09.124 |
| Citation | Mizushima Y, et al. (2017) Macrophage recruitment, but not interleukin 1 beta activation, enhances noise-induced hearing damage. Biochem Biophys Res Commun 493(2):894-900 |
| abstractText | 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-1beta), which noise exposure activated. However, IL-1beta 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-1beta inhibition does not reverse this cochlear damage. Therefore, macrophages may be a promising therapeutic target in human sensorineural hearing losses such as NIHL. |
