1. Macrophage recruitment, but not interleukin 1 beta activation, enhances noise-induced hearing damage.
- Author
-
Mizushima, Yu, Fujimoto, Chisato, Kashio, Akinori, Kondo, Kenji, and Yamasoba, Tatsuya
- Subjects
- *
NOISE-induced deafness , *MACROPHAGES , *INTERLEUKIN-1 , *HAIR cells , *GENE expression , *LABORATORY mice - Abstract
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. [ABSTRACT FROM AUTHOR]
- Published
- 2017
- Full Text
- View/download PDF