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The conversion of fibrinogen to fibrin at the surface of curliated E. coli bacteria leads to the generation of proinflammatory fibrinopeptides.

Persson, Kristin; Russell, Wayne LU ; Mörgelin, Matthias LU and Herwald, Heiko LU (2003) In Journal of Biological Chemistry 278(34). p.31884-31890
Abstract
The inflammatory response to bacterial infection is the result of a complex interplay between bacterial products and host effector systems, such as the immune and complement systems. Here we show that Escherichia coli bacteria expressing fibrous surface proteins, known as curli, assemble and activate factors of the human coagulation cascade at their surface. As a result of this interaction, fibrinogen is converted to fibrin and fibrinogen-derived peptides, termed fibrinopeptides, are generated. The molecular mechanisms behind the bacteria-induced formation of fibrinopeptides were investigated and shown to be triggered by the activation of the contact system, also known as the kallikrein/kinin system or the intrinsic pathway of coagulation.... (More)
The inflammatory response to bacterial infection is the result of a complex interplay between bacterial products and host effector systems, such as the immune and complement systems. Here we show that Escherichia coli bacteria expressing fibrous surface proteins, known as curli, assemble and activate factors of the human coagulation cascade at their surface. As a result of this interaction, fibrinogen is converted to fibrin and fibrinogen-derived peptides, termed fibrinopeptides, are generated. The molecular mechanisms behind the bacteria-induced formation of fibrinopeptides were investigated and shown to be triggered by the activation of the contact system, also known as the kallikrein/kinin system or the intrinsic pathway of coagulation. Samples containing fibrinopeptides generated by the interaction between bacteria and plasma were injected into animals and the inflammatory response was monitored. We found that this treatment provoked an infiltration of white blood cells, and the induction of the proinflammatory cytokine MCP-1 at the inflamed site. Our results therefore demonstrate that activation of the coagulation system at the bacterial surface contributes to the pathophysiology of bacterial infectious diseases. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Biological Chemistry
volume
278
issue
34
pages
31884 - 31890
publisher
ASBMB
external identifiers
  • wos:000184782100054
  • scopus:0041856152
ISSN
1083-351X
DOI
10.1074/jbc.M302522200
language
English
LU publication?
yes
id
56361f91-bb44-475d-8995-ab2153c7f99e (old id 115965)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12805381&dopt=Abstract
date added to LUP
2007-07-05 09:35:13
date last changed
2018-01-07 06:06:20
@article{56361f91-bb44-475d-8995-ab2153c7f99e,
  abstract     = {The inflammatory response to bacterial infection is the result of a complex interplay between bacterial products and host effector systems, such as the immune and complement systems. Here we show that Escherichia coli bacteria expressing fibrous surface proteins, known as curli, assemble and activate factors of the human coagulation cascade at their surface. As a result of this interaction, fibrinogen is converted to fibrin and fibrinogen-derived peptides, termed fibrinopeptides, are generated. The molecular mechanisms behind the bacteria-induced formation of fibrinopeptides were investigated and shown to be triggered by the activation of the contact system, also known as the kallikrein/kinin system or the intrinsic pathway of coagulation. Samples containing fibrinopeptides generated by the interaction between bacteria and plasma were injected into animals and the inflammatory response was monitored. We found that this treatment provoked an infiltration of white blood cells, and the induction of the proinflammatory cytokine MCP-1 at the inflamed site. Our results therefore demonstrate that activation of the coagulation system at the bacterial surface contributes to the pathophysiology of bacterial infectious diseases.},
  author       = {Persson, Kristin and Russell, Wayne and Mörgelin, Matthias and Herwald, Heiko},
  issn         = {1083-351X},
  language     = {eng},
  number       = {34},
  pages        = {31884--31890},
  publisher    = {ASBMB},
  series       = {Journal of Biological Chemistry},
  title        = {The conversion of fibrinogen to fibrin at the surface of curliated E. coli bacteria leads to the generation of proinflammatory fibrinopeptides.},
  url          = {http://dx.doi.org/10.1074/jbc.M302522200},
  volume       = {278},
  year         = {2003},
}