Hemolytic membrane vesicles of group B Streptococcus promote infection
B Armistead, P Quach, JM Snyder… - The Journal of …, 2021 - academic.oup.com
B Armistead, P Quach, JM Snyder, V Santana-Ufret, A Furuta, A Brokaw, L Rajagopal
The Journal of Infectious Diseases, 2021•academic.oup.comAbstract 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 …
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 …
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.
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