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J. Biol. Chem., Vol. 278, Issue 34, 31884-31890, August 22, 2003

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The Conversion of Fibrinogen to Fibrin at the Surface of Curliated Escherichia coli Bacteria Leads to the Generation of Proinflammatory Fibrinopeptides^*

Kristin Persson , Wayne Russell, Matthias Mörgelin and Heiko Herwald 

From the Department of Cell and Molecular Biology, Lund University, S-221 84 Lund, Sweden

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.

Received for publication, March 12, 2003 , and in revised form, June 1, 2003.

^* This work was supported in part by the foundations of Åke Wiberg, Alfred Österlund, Crafoord, Tore Nilson, Greta and Johan Kock, the Swedish Foundation for Strategic Research, King Gustaf V's 80-years fund, the Royal Physiographical Society in Lund, the Medical Faculty of Lund University, the Swedish Research Council (project 7480 and 13413), and Hansa Medical AB. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Supported by The Infection and Vaccinology program at the Swedish Foundation for Strategic Research.

To whom correspondence should be addressed: Dept. of Cell and Molecular Biology, Section for Molecular Pathogenesis, BMC, B14, Lund University, Tornavägen 10, SE-221 84 Lund, Sweden. Tel.: 46-46-2224182; Fax: 46-46-157756; E-mail: Heiko.Herwald{at}medkem.lu.se.

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