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Updated: Jul 13, 2026
A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
Published on: June 5, 2019
Differential kinetics and molecular recognition mechanisms involved in early versus late growth phase Staphylococcus
Niraj Procopio Evagrio George1, Konstantinos Konstantopoulos, Julia Myers Ross
1Department of Chemical and Biochemical Engineering, University of Maryland Baltimore County, Baltimore, MD 21250, USA.
Background:
Staphylococcus aureus adhesion to platelets via microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) is a critical first step in vascular infection. The molecular mechanisms governing adhesion are influenced by the repertoire of MSCRAMMs expressed on the bacterial surface and the fluid mechanical shear rates present in the vasculature. We compared the predominant adhesion mechanisms between early and late growth phase S. aureus under physiological shear conditions.
Methods:
A parallel-plate flow chamber was used to quantify the adhesion of early and late growth phase S. aureus to immobilized platelet layers as a function of wall shear rate. Specifically, we evaluated the influence of clumping factor (Clf) A, ClfB, serine-aspartate repeats, fibronectin-binding proteins (Fnbps), and protein A in supporting S. aureus adhesion to platelets. The ability of the plasma proteins fibrinogen and fibronectin to act as bridging molecules was also investigated.
Results:
Our results demonstrate a markedly elevated binding efficiency for late growth phase staphylococci to immobilized platelets, compared with that of the early growth phase cells in the high shear regime. During the late growth phase, fibrinogen in concert with von Willebrand factor (vWF) potentiates S. aureus-platelet binding via shear-dependent mechanisms. By contrast, fibrinogen, but not vWF, supports the adhesion of early growth phase S. aureus at the high wall shear rates. During the early growth phase, ClfA is identified as the dominant staphylococcal adhesion receptor, with Fnbps playing a supporting role.
Conclusion:
The results presented here demonstrate a differential mechanism and binding efficiency for the adhesion of early versus late growth phase S. aureus to immobilized platelets.
Insights
Staphylococcus aureus adhesion to platelets differs between early and late growth phases. Late-phase bacteria exhibit enhanced binding via fibrinogen and von Willebrand factor, while early-phase bacteria primarily use clumping factor A.
Area of Science:
- Microbiology
- Biophysics
- Vascular Biology
Background:
- Staphylococcus aureus adhesion to platelets is a key step in vascular infections.
- Bacterial adhesion mechanisms are influenced by surface proteins (MSCRAMMs) and blood flow (shear rates).
- Understanding these mechanisms is crucial for developing anti-adhesion therapies.
Purpose of the Study:
- To compare the primary adhesion mechanisms of early and late growth phase S. aureus to platelets.
- To investigate the role of specific MSCRAMMs and plasma proteins in S. aureus-platelet interactions under physiological shear conditions.
Main Methods:
- Utilized a parallel-plate flow chamber to assess S. aureus adhesion to platelets at varying shear rates.
- Quantified the contribution of clumping factor A (ClfA), ClfB, fibronectin-binding proteins (Fnbps), protein A, fibrinogen, and von Willebrand factor (vWF).
Main Results:
- Late growth phase S. aureus showed significantly higher binding efficiency to platelets than early growth phase cells under high shear.
- Fibrinogen and vWF promoted late-phase S. aureus binding, while fibrinogen alone supported early-phase binding.
- ClfA was the dominant adhesion receptor for early-phase S. aureus, with Fnbps playing a secondary role.
Conclusions:
- S. aureus exhibits distinct adhesion mechanisms and binding efficiencies to platelets depending on its growth phase.
- These findings highlight the dynamic nature of bacterial adhesion in the context of vascular infection.
