Hemolytic Membrane Vesicles of Group B Streptococcus Promote Infection.
granadaene
group B streptococcus
hemolysin
immune evasion
membrane vesicles
Journal
The Journal of infectious diseases
ISSN: 1537-6613
Titre abrégé: J Infect Dis
Pays: United States
ID NLM: 0413675
Informations de publication
Date de publication:
23 04 2021
23 04 2021
Historique:
received:
10
04
2020
accepted:
25
08
2020
pubmed:
30
8
2020
medline:
11
2
2022
entrez:
30
8
2020
Statut:
ppublish
Résumé
Group B streptococci (GBS) are β-hemolytic, Gram-positive bacteria associated with fetal injury, preterm birth, spontaneous abortion, and neonatal infections. A key factor promoting GBS virulence is the β-hemolysin/cytolysin, a pigmented ornithine rhamnolipid (also known as granadaene) associated with the bacterial surface. A previous study indicated that GBS produce small structures known as membrane vesicles (MVs), which contain virulence-associated proteins. In this study, we show that GBS MVs are pigmented and hemolytic, indicating that granadaene is functionally active in MVs. In addition, MVs from hyperhemolytic GBS induced greater cell death of neutrophils, T cells, and B cells compared with MVs from isogenic nonhemolytic GBS, implicating MVs as a potential mechanism for granadaene-mediated virulence. Finally, hemolytic MVs reduced oxidative killing of GBS and aggravated morbidity and mortality of neonatal mice infected with GBS. These studies, taken together, reveal a novel mechanism by which GBS deploy a crucial virulence factor to promote bacterial dissemination and pathogenesis.
Sections du résumé
BACKGROUND
Group B streptococci (GBS) are β-hemolytic, Gram-positive bacteria associated with fetal injury, preterm birth, spontaneous abortion, and neonatal infections. A key factor promoting GBS virulence is the β-hemolysin/cytolysin, a pigmented ornithine rhamnolipid (also known as granadaene) associated with the bacterial surface.
METHODS
A previous study indicated that GBS produce small structures known as membrane vesicles (MVs), which contain virulence-associated proteins. In this study, we show that GBS MVs are pigmented and hemolytic, indicating that granadaene is functionally active in MVs.
RESULTS
In addition, MVs from hyperhemolytic GBS induced greater cell death of neutrophils, T cells, and B cells compared with MVs from isogenic nonhemolytic GBS, implicating MVs as a potential mechanism for granadaene-mediated virulence. Finally, hemolytic MVs reduced oxidative killing of GBS and aggravated morbidity and mortality of neonatal mice infected with GBS.
CONCLUSIONS
These studies, taken together, reveal a novel mechanism by which GBS deploy a crucial virulence factor to promote bacterial dissemination and pathogenesis.
Identifiants
pubmed: 32861213
pii: 5899212
doi: 10.1093/infdis/jiaa548
pmc: PMC8064051
doi:
Substances chimiques
Bacterial Proteins
0
Hemolysin Proteins
0
Virulence Factors
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1488-1496Subventions
Organisme : NIAID NIH HHS
ID : T32 AI007509
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI145890
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI125907
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI133976
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI112619
Pays : United States
Organisme : NIAID NIH HHS
ID : T32 AI055396
Pays : United States
Informations de copyright
© The Author(s) 2020. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.
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