Bacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption

Bacterial meningitis remains a substantial cause of mortality worldwide and survivors may have severe lifelong disability. Although we know that meningeal bacterial pathogens must cross blood-central nervous system (CNS) barriers, the mechanisms which facilitate the virulence of these pathogens are...

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Autores principales:	Zunquan Zhao, Xueyi Shang, Ying Chen, Yuling Zheng, Wenhua Huang, Hua Jiang, Qingyu Lv, Decong Kong, Yongqiang Jiang, Peng Liu
Formato:	article
Lenguaje:	EN
Publicado:	Taylor & Francis Group 2020
Materias:	meningitis blood-brain barrier adenosine streptococcus suis streptococcus agalactiae brain microvascular endothelial cell central nervous system Infectious and parasitic diseases RC109-216
Acceso en línea:	https://doaj.org/article/2440c09ac2454d3bb9ff8cfab8221610
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spelling	oai:doaj.org-article:2440c09ac2454d3bb9ff8cfab82216102021-11-17T14:21:58ZBacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption2150-55942150-560810.1080/21505594.2020.1797352https://doaj.org/article/2440c09ac2454d3bb9ff8cfab82216102020-12-01T00:00:00Zhttp://dx.doi.org/10.1080/21505594.2020.1797352https://doaj.org/toc/2150-5594https://doaj.org/toc/2150-5608Bacterial meningitis remains a substantial cause of mortality worldwide and survivors may have severe lifelong disability. Although we know that meningeal bacterial pathogens must cross blood-central nervous system (CNS) barriers, the mechanisms which facilitate the virulence of these pathogens are poorly understood. Here, we show that adenosine from a surface enzyme (Ssads) of Streptococcus suis facilitates this pathogen’s entry into mouse brains. Monolayer translocation assays (from the human cerebrovascular endothelium) and experiments using diverse inhibitors and agonists together demonstrate that activation of the A1 adenosine receptor signaling cascade in hosts, as well as attendant cytoskeleton remodeling, promote S. suis penetration across blood-CNS barriers. Importantly, our additional findings showing that Ssads orthologs from other bacterial species also promote their translocation across barriers suggest that exploitation of A1 AR signaling may be a general mechanism of bacterial virulence.Zunquan ZhaoXueyi ShangYing ChenYuling ZhengWenhua HuangHua JiangQingyu LvDecong KongYongqiang JiangPeng LiuTaylor & Francis Grouparticlemeningitisblood-brain barrieradenosinestreptococcus suisstreptococcus agalactiaebrain microvascular endothelial cellcentral nervous systemInfectious and parasitic diseasesRC109-216ENVirulence, Vol 11, Iss 1, Pp 980-994 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	meningitis blood-brain barrier adenosine streptococcus suis streptococcus agalactiae brain microvascular endothelial cell central nervous system Infectious and parasitic diseases RC109-216
spellingShingle	meningitis blood-brain barrier adenosine streptococcus suis streptococcus agalactiae brain microvascular endothelial cell central nervous system Infectious and parasitic diseases RC109-216 Zunquan Zhao Xueyi Shang Ying Chen Yuling Zheng Wenhua Huang Hua Jiang Qingyu Lv Decong Kong Yongqiang Jiang Peng Liu Bacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption
description	Bacterial meningitis remains a substantial cause of mortality worldwide and survivors may have severe lifelong disability. Although we know that meningeal bacterial pathogens must cross blood-central nervous system (CNS) barriers, the mechanisms which facilitate the virulence of these pathogens are poorly understood. Here, we show that adenosine from a surface enzyme (Ssads) of Streptococcus suis facilitates this pathogen’s entry into mouse brains. Monolayer translocation assays (from the human cerebrovascular endothelium) and experiments using diverse inhibitors and agonists together demonstrate that activation of the A1 adenosine receptor signaling cascade in hosts, as well as attendant cytoskeleton remodeling, promote S. suis penetration across blood-CNS barriers. Importantly, our additional findings showing that Ssads orthologs from other bacterial species also promote their translocation across barriers suggest that exploitation of A1 AR signaling may be a general mechanism of bacterial virulence.
format	article
author	Zunquan Zhao Xueyi Shang Ying Chen Yuling Zheng Wenhua Huang Hua Jiang Qingyu Lv Decong Kong Yongqiang Jiang Peng Liu
author_facet	Zunquan Zhao Xueyi Shang Ying Chen Yuling Zheng Wenhua Huang Hua Jiang Qingyu Lv Decong Kong Yongqiang Jiang Peng Liu
author_sort	Zunquan Zhao
title	Bacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption
title_short	Bacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption
title_full	Bacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption
title_fullStr	Bacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption
title_full_unstemmed	Bacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption
title_sort	bacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption
publisher	Taylor & Francis Group
publishDate	2020
url	https://doaj.org/article/2440c09ac2454d3bb9ff8cfab8221610
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Bacteria elevate extracellular adenosine to exploit host signaling for blood-brain barrier disruption

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