title: Synthetic colloids attenuate leukocyte-endothelial interactions by inhibition of integrin function.
abstract: BACKGROUND
  It has been suspected that synthetic colloids may interfere with leukocyte adhesion by down-regulation of endothelial cell adhesion molecules. Although inhibition of endothelial inflammation might reduce leukocyte-related tissue injury, the same mechanism may be detrimental for host defense during severe infection. Regarding the widespread use of colloids, the authors performed a laboratory investigation to determine the mechanisms by which synthetic colloids interfere with leukocyte-endothelial interactions.
  
  
  METHODS
  Adhesion molecule expression on native and cytokine-activated endothelium from umbilical veins was measured after pretreatment with gelatin and various preparations of dextran or hydroxyethyl starch. Inhibition of neutrophil adhesion to activated endothelium was examined in a flow chamber by perfusion of untreated and colloid-treated neutrophils over colloid-pretreated endothelium at 2 dyn/cm. Comparisons were made between untreated controls, colloid-pretreated endothelium, and colloid-cotreated neutrophils.
  
  
  RESULTS
  Intercellular adhesion molecule 1, vascular cell adhesion molecule 1, E-selectin, and P-selectin were not attenuated by any colloid. Accordingly, colloid pretreatment of endothelium alone did not reduce neutrophil adhesion. In contrast, when neutrophils were cotreated by addition of colloids to the perfusate immediately before perfusion, adhesion decreased by 31-51% (P < 0.05) regardless of the colloid type. As indicated by the twofold increased rolling fractions, this reduction was due to an inhibition of neutrophil integrins.
  
  
  CONCLUSIONS
  This study shows that synthetic colloids inhibit neutrophil adhesion by a neutrophil-dependent mechanism rather than interfering with endothelial cell activation. This suggests that inhibition of leukocyte sequestration by volume support is a common and transient phenomenon depending on the colloid concentration in plasma.
authors.affiliation: Department of Anaesthesiology and Intensive Care Medicine, University Hospital, Eberhard-Karls University Tuebingen, Germany. boris.nohe@uni-tuebingen.de
authors.forename: Boris
authors.initials: B
authors.lastname: Nohé
authors.forename: Tanja
authors.initials: T
authors.lastname: Johannes
authors.forename: Jörg
authors.initials: J
authors.lastname: Reutershan
authors.forename: Albert
authors.initials: A
authors.lastname: Rothmund
authors.forename: Helene A
authors.initials: HA
authors.lastname: Haeberle
authors.forename: Annette
authors.initials: A
authors.lastname: Ploppa
authors.forename: Torsten H
authors.initials: TH
authors.lastname: Schroeder
authors.forename: Hans-Juergen
authors.initials: HJ
authors.lastname: Dieterich
mesh_terms: D002448:Cell Adhesion / Q000187:drug effects; D002450:Cell Communication / Q000187:drug effects*; D002478:Cells, Cultured; D003102:Colloids / Q000494:pharmacology*; D019040:E-Selectin / Q000097:blood; D042783:Endothelial Cells / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D016023:Integrins / Q000037:antagonists & inhibitors*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D009504:Neutrophils / Q000187:drug effects* / Q000502:physiology; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D003102:Colloids; D019040:E-Selectin; D016023:Integrins; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1