Toll-like receptor 2, hyaluronan, and neutrophils play a key role in plaque erosion: the OPTICO–acute coronary syndrome (ACS) study
Authors' conclusion
The current study provides first in-human evidence for distinct TLR2-mediated neutrophil activation in IFC-ACS, presumably triggered by elevated soluble hyaluronic acid.
Study context
- Population
- Patients with ACS from the OPTICO-ACS study; blood sampled at the culprit lesion and systemicallymatched
- Comparison
- IFC-ACS vs RFC-ACS
- IFC-ACSn = 32
- Outcome
- Neutrophil activation in IFC-ACS vs RFC-ACS (TLR2 expression, MMP9 release, endothelial cell death, hyaluronidase 2/hyaluronic acid)
Methodological detailsmatched
- Matched
Main finding
As reported in the abstract
- TLR2 expression higher on neutrophils from IFC-ACS than RFC-ACS patients
- TLR2 stimulation increased release of active MMP9 from local IFC-ACS-derived neutrophils
- IFC-ACS-derived neutrophils aggravated endothelial cell death independently of TLR2
- Thrombi of IFC-ACS patients exhibited more hyaluronidase 2, with increased local plasma hyaluronic acid (TLR2 ligand)
Original publication
Toll-like receptor 2, hyaluronan, and neutrophils play a key role in plaque erosion: the OPTICO–ACS study. Eur Heart J. Published 30 June 2023. doi:10.
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