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Interleukin-17 inhibits Adult Hippocampal Neurogenesis

Interleukin 17(A) (IL-17) is a potent pro-inflammatory cytokine that acts as a central regulator of inflammatory response within the brain, but its physiological roles under non-inflammatory conditions remain elusive. Here we report that endogenous IL-17 ablates neurogenesis in the adult dentate gyr...

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Detalles Bibliográficos
Autores principales: Liu, Qiang, Xin, Wei, He, Ping, Turner, Dharshaun, Yin, Junxiang, Gan, Yan, Shi, Fu-Dong, Wu, Jie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4271266/
https://www.ncbi.nlm.nih.gov/pubmed/25523081
http://dx.doi.org/10.1038/srep07554
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author Liu, Qiang
Xin, Wei
He, Ping
Turner, Dharshaun
Yin, Junxiang
Gan, Yan
Shi, Fu-Dong
Wu, Jie
author_facet Liu, Qiang
Xin, Wei
He, Ping
Turner, Dharshaun
Yin, Junxiang
Gan, Yan
Shi, Fu-Dong
Wu, Jie
author_sort Liu, Qiang
collection PubMed
description Interleukin 17(A) (IL-17) is a potent pro-inflammatory cytokine that acts as a central regulator of inflammatory response within the brain, but its physiological roles under non-inflammatory conditions remain elusive. Here we report that endogenous IL-17 ablates neurogenesis in the adult dentate gyrus (DG) of hippocampus. Genetic deletion of IL-17 increased the number of adult-born neurons in the DG. Further, we found that IL-17 deletion altered cytokine network, facilitated basal excitatory synaptic transmission, enhanced intrinsic neuronal excitability, and increased expression of proneuronal genes in neuronal progenitor cells (NPCs). Our findings suggest a profound role of IL-17 in the negative regulation of adult hippocampal neurogenesis under physiology conditions.
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spelling pubmed-42712662014-12-30 Interleukin-17 inhibits Adult Hippocampal Neurogenesis Liu, Qiang Xin, Wei He, Ping Turner, Dharshaun Yin, Junxiang Gan, Yan Shi, Fu-Dong Wu, Jie Sci Rep Article Interleukin 17(A) (IL-17) is a potent pro-inflammatory cytokine that acts as a central regulator of inflammatory response within the brain, but its physiological roles under non-inflammatory conditions remain elusive. Here we report that endogenous IL-17 ablates neurogenesis in the adult dentate gyrus (DG) of hippocampus. Genetic deletion of IL-17 increased the number of adult-born neurons in the DG. Further, we found that IL-17 deletion altered cytokine network, facilitated basal excitatory synaptic transmission, enhanced intrinsic neuronal excitability, and increased expression of proneuronal genes in neuronal progenitor cells (NPCs). Our findings suggest a profound role of IL-17 in the negative regulation of adult hippocampal neurogenesis under physiology conditions. Nature Publishing Group 2014-12-19 /pmc/articles/PMC4271266/ /pubmed/25523081 http://dx.doi.org/10.1038/srep07554 Text en Copyright © 2014, Macmillan Publishers Limited. All rights reserved http://creativecommons.org/licenses/by-nc-nd/4.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder in order to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/
spellingShingle Article
Liu, Qiang
Xin, Wei
He, Ping
Turner, Dharshaun
Yin, Junxiang
Gan, Yan
Shi, Fu-Dong
Wu, Jie
Interleukin-17 inhibits Adult Hippocampal Neurogenesis
title Interleukin-17 inhibits Adult Hippocampal Neurogenesis
title_full Interleukin-17 inhibits Adult Hippocampal Neurogenesis
title_fullStr Interleukin-17 inhibits Adult Hippocampal Neurogenesis
title_full_unstemmed Interleukin-17 inhibits Adult Hippocampal Neurogenesis
title_short Interleukin-17 inhibits Adult Hippocampal Neurogenesis
title_sort interleukin-17 inhibits adult hippocampal neurogenesis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4271266/
https://www.ncbi.nlm.nih.gov/pubmed/25523081
http://dx.doi.org/10.1038/srep07554
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