The conversion of fibrinogen to fibrin at the surface of curliated E. coli bacteria leads to the generation of proinflammatory fibrinopeptides.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/115965
- author
- Persson, Kristin ; Russell, Wayne LU ; Mörgelin, Matthias LU and Herwald, Heiko LU
- organization
- publishing date
- 2003
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of Biological Chemistry
- volume
- 278
- issue
- 34
- pages
- 31884 - 31890
- publisher
- American Society for Biochemistry and Molecular Biology
- 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
- 2016-04-01 12:21:19
- date last changed
- 2022-01-27 02:37:32
@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 = {{American Society for Biochemistry and Molecular Biology}}, 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}}, doi = {{10.1074/jbc.M302522200}}, volume = {{278}}, year = {{2003}}, }