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Platelet activation and aggregation by the opportunistic pathogen Cutibacterium (Propionibacterium) acnes
Frida Petersson1, Ola Kilsgård1,2, Oonagh Shannon1
1Division of Infection Medicine, Department of Clinical Sciences Lund, Lund University, Lund, Sweden.
Plos One
|February 1, 2018
Summary
Cutibacterium acnes, a skin bacterium, can aggregate platelets, a key immune cell, but this ability varies by bacterial type and donor plasma proteins. Specific proteins like IgG and fibrinogen are crucial for this interaction, impacting medical implant infections.
Area of Science:
- Microbiology
- Immunology
- Biochemistry
Background:
- Cutibacterium (Propionibacterium) acnes is a common skin bacterium and frequently found on medical implants.
- Its interaction with blood components, particularly platelets and plasma proteins, is not fully understood.
Purpose of the Study:
- To investigate the molecular mechanisms underlying the interaction between C. acnes and human platelets.
- To identify specific plasma proteins involved in C. acnes-mediated platelet aggregation.
Main Methods:
- Phylogenetic analysis of C. acnes isolates.
- Platelet aggregation assays.
- Mass spectrometry to identify plasma proteins.
- Fluorescence microscopy to visualize bacterial-platelet interactions.
Main Results:
- C. acnes phylotype influences platelet aggregation, with type IB isolates showing reduced ability.
- Plasma protein deposition on C. acnes is essential for platelet aggregation, reducing lag time.
- Identified IgG, fibrinogen, and complement factors as key deposited proteins.
- Inhibition of these proteins significantly decreased C. acnes-induced platelet aggregation.
Conclusions:
- C. acnes activates and aggregates platelets in a bacterium and donor-specific manner.
- Plasma proteins, including IgG, fibrinogen, and complement, are critical mediators of this interaction.
- Understanding these mechanisms provides insight into C. acnes pathogenesis on medical implants.
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