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Macrophages in Noise-Exposed Cochlea: Changes, Regulation and the Potential Role

Acoustic trauma is an important physical factor leading to cochlear damage and hearing impairments. Inflammation responds to this kind of cochlear damage stress. Macrophages, the major innate immune cells in the cochlea, are important drivers of inflammatory and tissue repair responses after cochlea...

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Detalles Bibliográficos
Autores principales: He, Weiwei, Yu, Jintao, Sun, Yu, Kong, Weijia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: JKL International LLC 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6961779/
https://www.ncbi.nlm.nih.gov/pubmed/32010492
http://dx.doi.org/10.14336/AD.2019.0723
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author He, Weiwei
Yu, Jintao
Sun, Yu
Kong, Weijia
author_facet He, Weiwei
Yu, Jintao
Sun, Yu
Kong, Weijia
author_sort He, Weiwei
collection PubMed
description Acoustic trauma is an important physical factor leading to cochlear damage and hearing impairments. Inflammation responds to this kind of cochlear damage stress. Macrophages, the major innate immune cells in the cochlea, are important drivers of inflammatory and tissue repair responses after cochlear injury. Recently, studies have shown that after noise exposure, the distribution, phenotype, and the number of cochlear macrophages have significantly changed, and the local environmental factors that shape macrophage differentiation and behavior are also drastically altered. However, the exact role of these immune cells in the cochlea after acoustic injury remains unknown. Here we review the properties of cochlear macrophages both under steady-state conditions and non-homeostatic conditions after cochlear acoustic injury and discuss their potential role in noise-exposed cochlea.
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spelling pubmed-69617792020-02-01 Macrophages in Noise-Exposed Cochlea: Changes, Regulation and the Potential Role He, Weiwei Yu, Jintao Sun, Yu Kong, Weijia Aging Dis Review Article Acoustic trauma is an important physical factor leading to cochlear damage and hearing impairments. Inflammation responds to this kind of cochlear damage stress. Macrophages, the major innate immune cells in the cochlea, are important drivers of inflammatory and tissue repair responses after cochlear injury. Recently, studies have shown that after noise exposure, the distribution, phenotype, and the number of cochlear macrophages have significantly changed, and the local environmental factors that shape macrophage differentiation and behavior are also drastically altered. However, the exact role of these immune cells in the cochlea after acoustic injury remains unknown. Here we review the properties of cochlear macrophages both under steady-state conditions and non-homeostatic conditions after cochlear acoustic injury and discuss their potential role in noise-exposed cochlea. JKL International LLC 2020-02-01 /pmc/articles/PMC6961779/ /pubmed/32010492 http://dx.doi.org/10.14336/AD.2019.0723 Text en Copyright: © 2019 He et al. http://creativecommons.org/licenses/by/2.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.
spellingShingle Review Article
He, Weiwei
Yu, Jintao
Sun, Yu
Kong, Weijia
Macrophages in Noise-Exposed Cochlea: Changes, Regulation and the Potential Role
title Macrophages in Noise-Exposed Cochlea: Changes, Regulation and the Potential Role
title_full Macrophages in Noise-Exposed Cochlea: Changes, Regulation and the Potential Role
title_fullStr Macrophages in Noise-Exposed Cochlea: Changes, Regulation and the Potential Role
title_full_unstemmed Macrophages in Noise-Exposed Cochlea: Changes, Regulation and the Potential Role
title_short Macrophages in Noise-Exposed Cochlea: Changes, Regulation and the Potential Role
title_sort macrophages in noise-exposed cochlea: changes, regulation and the potential role
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6961779/
https://www.ncbi.nlm.nih.gov/pubmed/32010492
http://dx.doi.org/10.14336/AD.2019.0723
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