gms | German Medical Science

Deutscher Kongress für Orthopädie und Unfallchirurgie
73. Jahrestagung der Deutschen Gesellschaft für Unfallchirurgie
95. Tagung der Deutschen Gesellschaft für Orthopädie und Orthopädische Chirurgie
50. Tagung des Berufsverbandes der Fachärzte für Orthopädie und Unfallchirurgie

21. - 24.10.2009, Berlin

Role for soluble fibrinogen to inhibit neutrophil adhesion and sequestration after trauma

Meeting Abstract

  • J. Pillay - Universitair Medisch Centrum Utrecht, Dept of Respiratory Medicine and Trauma, Utrecht, Netherlands
  • V. Kamp - Universitair Medisch Centrum Utrecht, Dept of Respiratory Medicine, Utrecht, Netherlands
  • L. Leenen - Universitair Medisch Centrum Utrecht, Dept of Trauma, Utrecht, Netherlands
  • L. Koenderman - Universitair Medisch Centrum Utrecht, Dept of Trauma, Utrecht, Netherlands
  • L. Ulfman - Universitair Medisch Centrum Utrecht, Dept of Respiratory Medicine, Utrecht, Netherlands

Deutscher Kongress für Orthopädie und Unfallchirurgie. 73. Jahrestagung der Deutschen Gesellschaft für Unfallchirurgie, 95. Tagung der Deutschen Gesellschaft für Orthopädie und Orthopädische Chirurgie, 50. Tagung des Berufsverbandes der Fachärzte für Orthopädie. Berlin, 21.-24.10.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. DocWI15-1325

DOI: 10.3205/09dkou135, URN: urn:nbn:de:0183-09dkou1359

Published: October 15, 2009

© 2009 Pillay et al.
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Outline

Text

Problem: Soluble fibrinogen (sFg) is an acute phase protein. In inflammation e.g. following trauma it increases up to 10 mg/ml.

Complications after trauma such as ARDS and MOF are mediated by neutrophils through adhesion to endothelial cells (EC) or sequestration in the vasculature: Adhesion-molecule dependent processes occur in post-capillary venules whereas adhesion-molecule independent retention occurs in micro-capillaries. The latter requires process F-actin polymerization of the neutrophil cytoskeleton. We show that sFg can reduce both types of neutrophil-EC interactions.

Method: Neutrophil adhesion to EC was studied in an in vitro flow-chamber. Cells, pre-incubated with various concentrations sFg or albumin, were perfused over TNF activated or chemokine presenting human umbilical vein endothelial cells (HUVEC) (1,5 dyn/cm2) and percentages of adhered cells were analyzed. F-actin polymerization was assessed by flow-cytometry.

Results and conclusions: Acute phase concentrations of sFg resulted in 20–30% adhered neutrophils on activated EC compared to albumin (60–70%). sFg did not decrease adherence in the presence of chemokines (IL-8/C5a). Neutrophils incubated with sFg appeared round, a feature of unactivated cells. sFg decreased the length of chemo-attractant-induced actin polymerization. sFg did not activate neutrophils, measured by intracellular [Ca2+], p-Erk or Nfκb phosphorylation.

Acute phase concentrations of sFg reduce neutrophil adherence and sequestration. Achievement of high plasma concentration of sFg directly after shock has the potential to reduce neutrophil adherence. Resuscitation using sFg or Fg-derived peptides might prevent ARDS and MOF.