Plasmin(ogen) acquisition by group A Streptococcus protects against C3b-mediated neutrophil killing

Ly, Diane, Taylor, Jude M., Tsatsaronis, James A., Monteleone, Mercedes M., Skora, Amanda S., Donald, Cortny A., Maddocks, Tracy, Nizet, Victor, West, Nicholas P., Ranson, Marie, Walker, Mark J., McArthur, Jason D. and Sanderson-Smith, Martina L. (2014) Plasmin(ogen) acquisition by group A Streptococcus protects against C3b-mediated neutrophil killing. Journal of Innate Immunity, 6 2: 240-250. doi:10.1159/000353754


Author Ly, Diane
Taylor, Jude M.
Tsatsaronis, James A.
Monteleone, Mercedes M.
Skora, Amanda S.
Donald, Cortny A.
Maddocks, Tracy
Nizet, Victor
West, Nicholas P.
Ranson, Marie
Walker, Mark J.
McArthur, Jason D.
Sanderson-Smith, Martina L.
Title Plasmin(ogen) acquisition by group A Streptococcus protects against C3b-mediated neutrophil killing
Formatted title
Plasmin(ogen) acquisition by group A Streptococcus protects against C3b-mediated neutrophil killing
Journal name Journal of Innate Immunity   Check publisher's open access policy
ISSN 1662-811X
1662-8128
Publication date 2014-02-01
Year available 2013
Sub-type Article (original research)
DOI 10.1159/000353754
Volume 6
Issue 2
Start page 240
End page 250
Total pages 11
Place of publication Basel, Switzerland
Publisher S. Karger
Language eng
Formatted abstract
The globally significant human pathogen group A Streptococcus (GAS) sequesters the host protease plasmin to the cell surface during invasive disease initiation. Recent evidence has shown that localized plasmin activity prevents opsonization of several bacterial species by key components of the innate immune system in vitro. Here we demonstrate that plasmin at the GAS cell surface resulted in degradation of complement factor C3b, and that plasminogen acquisition is associated with a decrease in C3b opsonization and neutrophil-mediated killing in vitro. Furthermore, the ability to acquire cell surface plasmin(ogen) correlates directly with a decrease in C3b opsonization, neutrophil phagocytosis, and increased bacterial survival in a humanized plasminogen mouse model of infection. These findings demonstrate that localized plasmin(ogen) plays an important role in facilitating GAS escape from the host innate immune response and increases bacterial virulence in the early stages of infection.
Keyword Complement
Innate immunity
M protein
Phagocytosis
Plasmin(ogen)
Streptococcus pyogenes

Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ
Additional Notes Published online: August 20, 2013

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2015 Collection
School of Chemistry and Molecular Biosciences
 
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Created: Fri, 28 Mar 2014, 19:34:06 EST by Mrs Louise Nimwegen on behalf of School of Chemistry & Molecular Biosciences