Brain-derived neurotrophic factor is regulated via MyD88/NF-κB signaling in experimental Streptococcus pneumoniae meningitis

Abstract Streptococcus pneumoniae meningitis is an intractable disease of the central nervous system (CNS). Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophic family and found to participate in the immune inflammatory response. In this study, we investigated if activation of th...

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Autores principales:	Danfeng Xu, Di Lian, Zhijie Zhang, Ying Liu, Jiaming Sun, Ling Li
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/2b4a57c9459741e29ae464c8962a5e98
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spelling	oai:doaj.org-article:2b4a57c9459741e29ae464c8962a5e982021-12-02T15:05:00ZBrain-derived neurotrophic factor is regulated via MyD88/NF-κB signaling in experimental Streptococcus pneumoniae meningitis10.1038/s41598-017-03861-z2045-2322https://doaj.org/article/2b4a57c9459741e29ae464c8962a5e982017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-03861-zhttps://doaj.org/toc/2045-2322Abstract Streptococcus pneumoniae meningitis is an intractable disease of the central nervous system (CNS). Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophic family and found to participate in the immune inflammatory response. In this study, we investigated if activation of the classical inflammatory signaling pathway, myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-κB), regulates BDNF expression in experimental S. pneumoniae meningitis. MyD88 knockout (myd88−/−) mice and wild-type littermates were infected intracisternally with S. pneumoniae suspension. Twenty-four hours after inoculation, histopathology of brains was evaluated. Cytokine and chemokine in brains and spleens was analyzed using ELISA. NF-κB activation was evaluated using EMSA. Cortical and hippocampal BDNF was assessed using RT-PCR and ELISA, respectively. BDNF promoter activity was evaluated using ChIP-PCR. myd88−/− mice showed an obviously weakened inflammatory host response. This diminished inflammation was consistent with worse clinical parameters, neuron injury, and apoptosis. Deficiency in MyD88 was associated with decreased BDNF expression. Furthermore, we identified a valid κB-binding site in the BDNF promoter, consistent with activation of NF-κB induced by inflammation. To sum up, MyD88/NF-κB signaling has a crucial role in up-regulating BDNF, which might provide potential therapeutic targets for S. pneumoniae meningitis.Danfeng XuDi LianZhijie ZhangYing LiuJiaming SunLing LiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-10 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Danfeng Xu Di Lian Zhijie Zhang Ying Liu Jiaming Sun Ling Li Brain-derived neurotrophic factor is regulated via MyD88/NF-κB signaling in experimental Streptococcus pneumoniae meningitis
description	Abstract Streptococcus pneumoniae meningitis is an intractable disease of the central nervous system (CNS). Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophic family and found to participate in the immune inflammatory response. In this study, we investigated if activation of the classical inflammatory signaling pathway, myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-κB), regulates BDNF expression in experimental S. pneumoniae meningitis. MyD88 knockout (myd88−/−) mice and wild-type littermates were infected intracisternally with S. pneumoniae suspension. Twenty-four hours after inoculation, histopathology of brains was evaluated. Cytokine and chemokine in brains and spleens was analyzed using ELISA. NF-κB activation was evaluated using EMSA. Cortical and hippocampal BDNF was assessed using RT-PCR and ELISA, respectively. BDNF promoter activity was evaluated using ChIP-PCR. myd88−/− mice showed an obviously weakened inflammatory host response. This diminished inflammation was consistent with worse clinical parameters, neuron injury, and apoptosis. Deficiency in MyD88 was associated with decreased BDNF expression. Furthermore, we identified a valid κB-binding site in the BDNF promoter, consistent with activation of NF-κB induced by inflammation. To sum up, MyD88/NF-κB signaling has a crucial role in up-regulating BDNF, which might provide potential therapeutic targets for S. pneumoniae meningitis.
format	article
author	Danfeng Xu Di Lian Zhijie Zhang Ying Liu Jiaming Sun Ling Li
author_facet	Danfeng Xu Di Lian Zhijie Zhang Ying Liu Jiaming Sun Ling Li
author_sort	Danfeng Xu
title	Brain-derived neurotrophic factor is regulated via MyD88/NF-κB signaling in experimental Streptococcus pneumoniae meningitis
title_short	Brain-derived neurotrophic factor is regulated via MyD88/NF-κB signaling in experimental Streptococcus pneumoniae meningitis
title_full	Brain-derived neurotrophic factor is regulated via MyD88/NF-κB signaling in experimental Streptococcus pneumoniae meningitis
title_fullStr	Brain-derived neurotrophic factor is regulated via MyD88/NF-κB signaling in experimental Streptococcus pneumoniae meningitis
title_full_unstemmed	Brain-derived neurotrophic factor is regulated via MyD88/NF-κB signaling in experimental Streptococcus pneumoniae meningitis
title_sort	brain-derived neurotrophic factor is regulated via myd88/nf-κb signaling in experimental streptococcus pneumoniae meningitis
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/2b4a57c9459741e29ae464c8962a5e98
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Brain-derived neurotrophic factor is regulated via MyD88/NF-κB signaling in experimental Streptococcus pneumoniae meningitis

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