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Venous shear stress enhances platelet mediated staphylococcal adhesion to artificial and damaged biological surfaces.

Fallgren, Corina; Ljungh, Åsa LU ; Shenkman, Boris; Varon, David and Savion, Naphtali (2002) In Biomaterials 23(23). p.4581-4589
Abstract
We investigated the role of blood components in the adhesion of staphylococci to biological and artificial surfaces under well-defined flow conditions by using the Cone and Plate(let) Analyzer. An enzyme-linked immunosorbent assay-like binding assay with biotinylated bacteria determined the extent of bacterial adhesion to subendothelial extracellular matrix (ECM), polystyrene (PS) and adult bovine aortic endothelial (ABAE) cell monolayer. The presence of adsorbed plasma proteins on PS and ECM did not increase and in some cases reduced staphylococcal adhesion under flow conditions (200s(-1)). However, their presence on ABAE cells increased bacterial adhesion but to a level still lower than the adhesion to PS and ECM. In contrast, adhered... (More)
We investigated the role of blood components in the adhesion of staphylococci to biological and artificial surfaces under well-defined flow conditions by using the Cone and Plate(let) Analyzer. An enzyme-linked immunosorbent assay-like binding assay with biotinylated bacteria determined the extent of bacterial adhesion to subendothelial extracellular matrix (ECM), polystyrene (PS) and adult bovine aortic endothelial (ABAE) cell monolayer. The presence of adsorbed plasma proteins on PS and ECM did not increase and in some cases reduced staphylococcal adhesion under flow conditions (200s(-1)). However, their presence on ABAE cells increased bacterial adhesion but to a level still lower than the adhesion to PS and ECM. In contrast, adhered platelets significantly increased staphylococcal adhesion to both PS and ECM, but did not affect the adhesion to ABAE cells. Furthermore, bacterial adhesion to the platelets coated ECM and PS under flow conditions (200s(-1)) was increased by 1.4 to 2.6-fold compare to static conditions. The platelet-enhanced bacterial adhesion was markedly inhibited by blockade of the platelet GPIb receptor. In conclusion, staphylococcal extensive adhesion to ECM and PS surfaces is increased by venous flow and mediated by surface adhered activated platelets via a GPIb dependent mechanism. On the other hand, ABAE cells demonstrated limited bacterial adhesion that is mediated by adsorbed plasma proteins. Our results suggest that under physiological venous flow conditions the intact vessel wall is less prone for bacterial adhesion than damaged vessel wall. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Biomaterials
volume
23
issue
23
pages
4581 - 4589
publisher
Elsevier
external identifiers
  • wos:000178116900018
  • pmid:12322979
  • scopus:0036970814
ISSN
1878-5905
DOI
10.1016/S0142-9612(02)00204-1
language
English
LU publication?
yes
id
8168f8b9-4980-4826-aea0-41ae53079a67 (old id 110175)
date added to LUP
2007-07-09 15:49:09
date last changed
2017-01-01 04:21:51
@article{8168f8b9-4980-4826-aea0-41ae53079a67,
  abstract     = {We investigated the role of blood components in the adhesion of staphylococci to biological and artificial surfaces under well-defined flow conditions by using the Cone and Plate(let) Analyzer. An enzyme-linked immunosorbent assay-like binding assay with biotinylated bacteria determined the extent of bacterial adhesion to subendothelial extracellular matrix (ECM), polystyrene (PS) and adult bovine aortic endothelial (ABAE) cell monolayer. The presence of adsorbed plasma proteins on PS and ECM did not increase and in some cases reduced staphylococcal adhesion under flow conditions (200s(-1)). However, their presence on ABAE cells increased bacterial adhesion but to a level still lower than the adhesion to PS and ECM. In contrast, adhered platelets significantly increased staphylococcal adhesion to both PS and ECM, but did not affect the adhesion to ABAE cells. Furthermore, bacterial adhesion to the platelets coated ECM and PS under flow conditions (200s(-1)) was increased by 1.4 to 2.6-fold compare to static conditions. The platelet-enhanced bacterial adhesion was markedly inhibited by blockade of the platelet GPIb receptor. In conclusion, staphylococcal extensive adhesion to ECM and PS surfaces is increased by venous flow and mediated by surface adhered activated platelets via a GPIb dependent mechanism. On the other hand, ABAE cells demonstrated limited bacterial adhesion that is mediated by adsorbed plasma proteins. Our results suggest that under physiological venous flow conditions the intact vessel wall is less prone for bacterial adhesion than damaged vessel wall.},
  author       = {Fallgren, Corina and Ljungh, Åsa and Shenkman, Boris and Varon, David and Savion, Naphtali},
  issn         = {1878-5905},
  language     = {eng},
  number       = {23},
  pages        = {4581--4589},
  publisher    = {Elsevier},
  series       = {Biomaterials},
  title        = {Venous shear stress enhances platelet mediated staphylococcal adhesion to artificial and damaged biological surfaces.},
  url          = {http://dx.doi.org/10.1016/S0142-9612(02)00204-1},
  volume       = {23},
  year         = {2002},
}