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Active but inoperable thrombin is accumulated in a plasma protein layer surrounding Streptococcus pyogenes.

Naudin, Clément LU ; Hurley, Sinead LU ; Malmström, Erik LU ; Plug, T; Shannon, Oonagh LU ; Meijers, J C M; Mörgelin, Matthias LU ; Björck, Lars LU and Herwald, Heiko LU (2015) In Thrombosis and Haemostasis 114(4). p.717-726
Abstract
Activation of thrombin is a critical determinant in many physiological and pathological processes including haemostasis and inflammation. Under physiological conditions many of these functions are involved in wound healing or eradication of an invading pathogen. However, when activated systemically, thrombin can contribute to severe and life-threatening conditions by causing complications such as multiple multi-organ failure and disseminated intravascular coagulation. In the present study we investigated how the activity of thrombin is modulated when it is bound to the surface of Streptococcus pyogenes. Our data show that S. pyogenes bacteria become covered with a proteinaceous layer when incubated with human plasma, and that thrombin is a... (More)
Activation of thrombin is a critical determinant in many physiological and pathological processes including haemostasis and inflammation. Under physiological conditions many of these functions are involved in wound healing or eradication of an invading pathogen. However, when activated systemically, thrombin can contribute to severe and life-threatening conditions by causing complications such as multiple multi-organ failure and disseminated intravascular coagulation. In the present study we investigated how the activity of thrombin is modulated when it is bound to the surface of Streptococcus pyogenes. Our data show that S. pyogenes bacteria become covered with a proteinaceous layer when incubated with human plasma, and that thrombin is a constituent of this layer. Though the coagulation factor is found attached to the bacteria with a functional active site, thrombin has lost its capacity to interact with its natural substrates and inhibitors. Thus, the interaction of bacteria with human plasma renders thrombin completely inoperable at the streptococcal surface. This could represent a host defense mechanism to avoid systemic activation of coagulation which could be otherwise induced when bacteria enter the circulation and cause systemic infection. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Thrombosis and Haemostasis
volume
114
issue
4
pages
717 - 726
publisher
F K Schattauer Verlag Gmbh
external identifiers
  • pmid:25994766
  • wos:000362144300009
  • scopus:84943169549
ISSN
0340-6245
DOI
10.1160/TH15-02-0127
language
English
LU publication?
yes
id
bd3968ca-6a2a-43db-b5ca-6da61577885b (old id 5448402)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/25994766?dopt=Abstract
date added to LUP
2015-06-05 11:48:48
date last changed
2017-01-01 06:35:17
@article{bd3968ca-6a2a-43db-b5ca-6da61577885b,
  abstract     = {Activation of thrombin is a critical determinant in many physiological and pathological processes including haemostasis and inflammation. Under physiological conditions many of these functions are involved in wound healing or eradication of an invading pathogen. However, when activated systemically, thrombin can contribute to severe and life-threatening conditions by causing complications such as multiple multi-organ failure and disseminated intravascular coagulation. In the present study we investigated how the activity of thrombin is modulated when it is bound to the surface of Streptococcus pyogenes. Our data show that S. pyogenes bacteria become covered with a proteinaceous layer when incubated with human plasma, and that thrombin is a constituent of this layer. Though the coagulation factor is found attached to the bacteria with a functional active site, thrombin has lost its capacity to interact with its natural substrates and inhibitors. Thus, the interaction of bacteria with human plasma renders thrombin completely inoperable at the streptococcal surface. This could represent a host defense mechanism to avoid systemic activation of coagulation which could be otherwise induced when bacteria enter the circulation and cause systemic infection.},
  author       = {Naudin, Clément and Hurley, Sinead and Malmström, Erik and Plug, T and Shannon, Oonagh and Meijers, J C M and Mörgelin, Matthias and Björck, Lars and Herwald, Heiko},
  issn         = {0340-6245},
  language     = {eng},
  number       = {4},
  pages        = {717--726},
  publisher    = {F K Schattauer Verlag Gmbh},
  series       = {Thrombosis and Haemostasis},
  title        = {Active but inoperable thrombin is accumulated in a plasma protein layer surrounding Streptococcus pyogenes.},
  url          = {http://dx.doi.org/10.1160/TH15-02-0127},
  volume       = {114},
  year         = {2015},
}