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Blockade of tissue factor-factor X binding attenuates sepsis-induced respiratory and renal failure.

Publication ,  Journal Article
Welty-Wolf, KE; Carraway, MS; Ortel, TL; Ghio, AJ; Idell, S; Egan, J; Zhu, X; Jiao, J-A; Wong, HC; Piantadosi, CA
Published in: Am J Physiol Lung Cell Mol Physiol
January 2006

Tissue factor expression in sepsis activates coagulation in the lung, which potentiates inflammation and leads to fibrin deposition. We hypothesized that blockade of factor X binding to the tissue factor-factor VIIa complex would prevent sepsis-induced damage to the lungs and other organs. Acute lung injury was produced in 15 adult baboons primed with killed Escherichia coli [1 x 10(9) colony-forming units (CFU)/kg], and then 12 h later, they were given 1 x 10(10) CFU/kg live E. coli by infusion. Two hours after live E. coli, animals received antibiotics with or without monoclonal antibody to tissue factor intravenously to block tissue factor-factor X binding. The animals were monitored physiologically for 34 h before being killed and their tissue harvested. The antibody treatment attenuated abnormalities in gas exchange and lung compliance, preserved renal function, and prevented tissue neutrophil influx and bowel edema relative to antibiotics alone (all P < 0.05). It also attenuated fibrinogen depletion (P < 0.01) and decreased proinflammatory cytokines, e.g., IL-6 and -8 (P < 0.01), in systemic and alveolar compartments. Similar protective effects of the antibody on IL-6 and -8 expression and permeability were found in lipopolysaccharide-stimulated endothelial cells. Blockade of factor X binding to the tissue factor-factor VIIa complex attenuates lung and organ injuries in established E. coli sepsis by attenuating the neutrophilic response and inflammatory pathways.

Duke Scholars

Published In

Am J Physiol Lung Cell Mol Physiol

DOI

ISSN

1040-0605

Publication Date

January 2006

Volume

290

Issue

1

Start / End Page

L21 / L31

Location

United States

Related Subject Headings

  • Thromboplastin
  • Respiratory System
  • Respiratory Insufficiency
  • Renal Insufficiency
  • Papio
  • Male
  • Lipopolysaccharides
  • Inflammation Mediators
  • Immunoglobulin Fab Fragments
  • Humans
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Welty-Wolf, K. E., Carraway, M. S., Ortel, T. L., Ghio, A. J., Idell, S., Egan, J., … Piantadosi, C. A. (2006). Blockade of tissue factor-factor X binding attenuates sepsis-induced respiratory and renal failure. Am J Physiol Lung Cell Mol Physiol, 290(1), L21–L31. https://doi.org/10.1152/ajplung.00155.2005
Welty-Wolf, Karen E., Martha S. Carraway, Thomas L. Ortel, Andrew J. Ghio, Steven Idell, Jack Egan, Xiaoyun Zhu, Jin-an Jiao, Hing C. Wong, and Claude A. Piantadosi. “Blockade of tissue factor-factor X binding attenuates sepsis-induced respiratory and renal failure.Am J Physiol Lung Cell Mol Physiol 290, no. 1 (January 2006): L21–31. https://doi.org/10.1152/ajplung.00155.2005.
Welty-Wolf KE, Carraway MS, Ortel TL, Ghio AJ, Idell S, Egan J, et al. Blockade of tissue factor-factor X binding attenuates sepsis-induced respiratory and renal failure. Am J Physiol Lung Cell Mol Physiol. 2006 Jan;290(1):L21–31.
Welty-Wolf, Karen E., et al. “Blockade of tissue factor-factor X binding attenuates sepsis-induced respiratory and renal failure.Am J Physiol Lung Cell Mol Physiol, vol. 290, no. 1, Jan. 2006, pp. L21–31. Pubmed, doi:10.1152/ajplung.00155.2005.
Welty-Wolf KE, Carraway MS, Ortel TL, Ghio AJ, Idell S, Egan J, Zhu X, Jiao J-A, Wong HC, Piantadosi CA. Blockade of tissue factor-factor X binding attenuates sepsis-induced respiratory and renal failure. Am J Physiol Lung Cell Mol Physiol. 2006 Jan;290(1):L21–L31.

Published In

Am J Physiol Lung Cell Mol Physiol

DOI

ISSN

1040-0605

Publication Date

January 2006

Volume

290

Issue

1

Start / End Page

L21 / L31

Location

United States

Related Subject Headings

  • Thromboplastin
  • Respiratory System
  • Respiratory Insufficiency
  • Renal Insufficiency
  • Papio
  • Male
  • Lipopolysaccharides
  • Inflammation Mediators
  • Immunoglobulin Fab Fragments
  • Humans