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Updated: Mar 28, 2026

In Vitro and In Vivo Model to Study Bacterial Adhesion to the Vessel Wall Under Flow Conditions
Published on: June 11, 2015
Coordinated Molecular Cross-Talk between Staphylococcus aureus, Endothelial Cells and Platelets in Bloodstream
Carolina D Garciarena1, Tony M McHale2, Rebecca L Watkin3
1Cardiovascular Infection Research Group, School of Pharmacy & Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, 123 St. Stephen's Green, Dublin 2, Ireland. carolinagarciarena@rcsi.ie.
Abstract:
Staphylococcus aureus is an opportunistic pathogen often carried asymptomatically on the human body. Upon entry to the otherwise sterile environment of the cardiovascular system, S. aureus can lead to serious complications resulting in organ failure and death. The success of S. aureus as a pathogen in the bloodstream is due to its ability to express a wide array of cell wall proteins on its surface that recognise host receptors, extracellular matrix proteins and plasma proteins. Endothelial cells and platelets are important cells in the cardiovascular system and are a major target of bloodstream infection. Endothelial cells form the inner lining of a blood vessel and provide an antithrombotic barrier between the vessel wall and blood. Platelets on the other hand travel throughout the cardiovascular system and respond by aggregating around the site of injury and initiating clot formation. Activation of either of these cells leads to functional dysregulation in the cardiovascular system. In this review, we will illustrate how S. aureus establish intimate interactions with both endothelial cells and platelets leading to cardiovascular dysregulation.
Insights
Staphylococcus aureus bloodstream infections disrupt cardiovascular function by interacting with endothelial cells and platelets. This pathogen exploits cell wall proteins to cause serious complications, including organ failure.
Area of Science:
- Cardiovascular Science
- Infectious Disease
- Microbiology
Background:
- Staphylococcus aureus is an opportunistic pathogen that can cause severe bloodstream infections.
- The cardiovascular system, including endothelial cells and platelets, is a primary target for S. aureus.
- S. aureus utilizes surface cell wall proteins to interact with host components, facilitating infection.
Purpose of the Study:
- To review the mechanisms by which Staphylococcus aureus interacts with endothelial cells and platelets.
- To elucidate how these interactions lead to cardiovascular dysregulation during bloodstream infections.
Main Methods:
- This review synthesizes existing research on S. aureus interactions with cardiovascular components.
- Literature analysis focusing on molecular mechanisms of pathogen-host cell engagement.
Main Results:
- Staphylococcus aureus employs surface proteins to bind to endothelial cells and platelets.
- These interactions trigger the activation and functional dysregulation of endothelial cells and platelets.
- Such dysregulation contributes to the pathogenesis of S. aureus bloodstream infections.
Conclusions:
- Staphylococcus aureus establishes critical interactions with endothelial cells and platelets.
- These interactions are key to S. aureus pathogenesis in the cardiovascular system.
- Understanding these interactions is vital for developing strategies against S. aureus bloodstream infections.
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