Lower level noise exposure that produces only TTS modulates the immune homeostasis of cochlear macrophages.

Lower level noise exposure that produces only TTS modulates the immune homeostasis of cochlear macrophages.
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DOI:
10.1016/j.jneuroim.2018.06.019
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发表时间:
2018-10-15
影响因子:
3.3
通讯作者:
Hu BH
Hu BH
中科院分区:
医学4区
文献类型:
--
作者:
Frye MD;Zhang C;Hu BH

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噪声暴露产生的暂时性阈值偏移(TTS)已被证明会导致耳蜗生理和听力功能的永久性变化。耳蜗功能的这些长期变化有几种解释,例如感觉细胞静纤毛和感觉细胞与螺旋神经节神经元的神经支配之间的突触连接受损,以及听神经的脱髓鞘。虽然这些结构缺陷与听力困难有关,但耳蜗对这种应力损伤的反应仍然知之甚少。在这里,我们报告了暴露于仅导致TTS的低水平噪音(LLN)后耳蜗免疫系统的激活。使用多种形态学、分子和功能参数,我们评估了巨噬细胞(耳蜗中的主要免疫细胞群)对LLN暴露的反应。这项研究表明,一个LLN,导致只有TTS增加巨噬细胞的数量在耳蜗区紧邻感觉细胞和它们的神经支配。这些细胞中的许多获得活化形态并表达对巨噬细胞炎症活性和粘附重要的免疫分子CCL2和ICAM 1。然而,LLN暴露降低巨噬细胞吞噬能力。虽然耳蜗巨噬细胞的活化形态逆转,但在LLN暴露后2个月未实现完全恢复。综上所述,这些观察结果清楚地表明耳蜗免疫系统参与了对LLN的耳蜗反应,不会导致永久性阈值变化。
Noise exposure producing temporary threshold shifts (TTS) has been demonstrated to cause permanent changes to cochlear physiology and hearing function. Several explanations have been purported to underlie these long-term changes in cochlear function, such as damage to sensory cell stereocilia and synaptic connections between sensory cells and their innervation by spiral ganglion neurons, and demyelination of the auditory nerve. Though these structural defects have been implicated in hearing difficulty, cochlear responses to this stress damage remains poorly understood. Here, we report the activation of the cochlear immune system following exposure to lower level noise (LLN) that causes only TTS. Using multiple morphological, molecular and functional parameters, we assessed the responses of macrophages, the primary immune cell population in the cochlea, to the LLN exposure. This study reveals that a LLN that causes only TTS increases the macrophage population in cochlear regions immediately adjacent to sensory cells and their innervations. Many of these cells acquire an activated morphology and express the immune molecules CCL2 and ICAM1 that are important for macrophage inflammatory activity and adhesion. However, LLN exposure reduces macrophage phagocytic ability. While the activated morphology of cochlear macrophages reverses, the complete recovery is not achieved 2 months after the LLN exposure. Taken together, these observations clearly implicate the cochlear immune system in the cochlear response to LLN that causes no permanent threshold change.
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