The Journal of Experimental Medicine
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Published online 20 November 2000.
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© The Rockefeller University Press, 0022-1007/2000/11/1415/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 10, November 20, 2000 1415-1424

Original Article

Severe Lung Lesions Caused by Salmonella Are Prevented by Inhibition of the Contact System

Kristin Perssona, Matthias Mörgelina, Lennart Lindbomc, Per Almb, Lars Björcka, and Heiko Herwalda

a Department of Cell and Molecular Biology, Lund University, S-221 00 Lund, Sweden
b Department of Pathology, Lund University, S-221 00 Lund, Sweden
c Department of Physiology and Pharmacology, Karolinska Institute, S-171 77 Stockholm, Sweden
Department of Cell and Molecular Biology, Section for Molecular Pathogenesis, Lund University, P.O. Box 94, S-221 00 Lund, Sweden.46-46-15775646-46-2224488

Vascular damage induced by trauma, inflammation, or infection results in an alteration of the endothelium from a nonactivated to a procoagulant, vasoconstrictive, and proinflammatory state, and can lead to life-threatening complications. Here we report that activation of the contact system by Salmonella leads to massive infiltration of red blood cells and fibrin deposition in the lungs of infected rats. These pulmonary lesions were prevented when the infected animals were treated with H-D-Pro-Phe-Arg-chloromethylketone, an inhibitor of coagulation factor XII and plasma kallikrein, suggesting that inhibition of contact system activation could be used therapeutically in severe infectious disease.

Key Words: bradykinin • factor XII • high molecular weight kininogen • plasma kallikrein • protease inhibitor

K. Persson and M. Mörgelin contributed equally to this work.

Abbreviations used in this paper: aPTT, activated partial thromboplastin time; F, factor; HK, H-kininogen; PK, plasma kallikrein; PT, prothrombin.

© 2000 The Rockefeller University Press


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