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Group G streptococci mediate fibrinogendependent platelet aggregation leading to transient entrapment in platelet aggregates

Svensson, Lisbeth LU ; Frick, Inga-Maria LU and Shannon, Oonagh LU (2016) In Microbiology 162(1). p.117-126
Abstract

Platelets have been reported to become activated in response to bacteria and this is proposed to contribute to the acute response to bacterial infection. In the present study, we investigated platelet aggregation in response to group G streptococci (GGS) in vitro in healthy human donors and in vivo in a mouse model of streptococcal sepsis. Platelet aggregation by GGS was dependent on the bacterial surface protein FOG and engagement of the platelet fibrinogen receptor; however, it was independent of IgG and the platelet Fc receptor. Platelets exerted no antibacterial effects on the bacteria, and aggregates formed were markedly unstable, allowing bacteria to rapidly return to the plasma and grow post-aggregation. Thrombocytopenia and... (More)

Platelets have been reported to become activated in response to bacteria and this is proposed to contribute to the acute response to bacterial infection. In the present study, we investigated platelet aggregation in response to group G streptococci (GGS) in vitro in healthy human donors and in vivo in a mouse model of streptococcal sepsis. Platelet aggregation by GGS was dependent on the bacterial surface protein FOG and engagement of the platelet fibrinogen receptor; however, it was independent of IgG and the platelet Fc receptor. Platelets exerted no antibacterial effects on the bacteria, and aggregates formed were markedly unstable, allowing bacteria to rapidly return to the plasma and grow post-aggregation. Thrombocytopenia and platelet activation occurred during invasive infection with GGS, and platelets were demonstrated to contribute to bacterial dissemination during infection. These findings reveal an important role for bacteria–platelet interactions during the pathogenesis of streptococcal infection.

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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
G streptococci , platelet aggregation
in
Microbiology
volume
162
issue
1
pages
10 pages
publisher
MAIK Nauka/Interperiodica
external identifiers
  • Scopus:84957352956
ISSN
1350-0872
DOI
10.1099/mic.0.000203
language
English
LU publication?
yes
id
85b18600-67dd-48a1-8b7b-7831db22691d
date added to LUP
2016-06-16 10:51:53
date last changed
2016-09-20 03:19:55
@misc{85b18600-67dd-48a1-8b7b-7831db22691d,
  abstract     = {<p>Platelets have been reported to become activated in response to bacteria and this is proposed to contribute to the acute response to bacterial infection. In the present study, we investigated platelet aggregation in response to group G streptococci (GGS) in vitro in healthy human donors and in vivo in a mouse model of streptococcal sepsis. Platelet aggregation by GGS was dependent on the bacterial surface protein FOG and engagement of the platelet fibrinogen receptor; however, it was independent of IgG and the platelet Fc receptor. Platelets exerted no antibacterial effects on the bacteria, and aggregates formed were markedly unstable, allowing bacteria to rapidly return to the plasma and grow post-aggregation. Thrombocytopenia and platelet activation occurred during invasive infection with GGS, and platelets were demonstrated to contribute to bacterial dissemination during infection. These findings reveal an important role for bacteria–platelet interactions during the pathogenesis of streptococcal infection.</p>},
  author       = {Svensson, Lisbeth and Frick, Inga-Maria and Shannon, Oonagh},
  issn         = {1350-0872},
  keyword      = {G streptococci ,platelet aggregation },
  language     = {eng},
  month        = {01},
  number       = {1},
  pages        = {117--126},
  publisher    = {ARRAY(0x7972fe8)},
  series       = {Microbiology},
  title        = {Group G streptococci mediate fibrinogendependent platelet aggregation leading to transient entrapment in platelet aggregates},
  url          = {http://dx.doi.org/10.1099/mic.0.000203},
  volume       = {162},
  year         = {2016},
}