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

Authors
  • Zhao, Zunquan1
  • Shang, Xueyi1, 2
  • Chen, Ying3
  • Zheng, Yuling1
  • Huang, Wenhua1
  • Jiang, Hua1
  • Lv, Qingyu1
  • Kong, Decong1
  • Jiang, Yongqiang1
  • Liu, Peng1
  • 1 State Key Laboratory of Pathogens and Biosecurity, Institute of Microbiology and Epidemiology , Beijing, China. , (China)
  • 2 Department of Critical Care Medicine, The Fifth Medical Center of Chinese PLA General Hospital , Beijing, China. , (China)
  • 3 School of Food and Chemical Engineering, Beijing Technology and Business University , Beijing, China. , (China)
Type
Published Article
Journal
Virulence
Publisher
Landes Bioscience
Publication Date
Dec 01, 2020
Volume
11
Issue
1
Pages
980–994
Identifiers
DOI: 10.1080/21505594.2020.1797352
PMID: 32772676
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

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.

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