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Reciprocal activation of leukocyte-endothelial adhesion molecules in acute coronary syndromes
Ross T Murphy1, J B Foley, Peter Crean
1Department of Cardiology, St James's Hospital, Dublin 8, Ireland. rmurphy@sghms.ac.uk
Insights
Acute coronary syndromes involve inflammation and leukocyte activation. Studies show elevated monocyte markers and adhesion molecules, suggesting a systemic inflammatory source in acute coronary disease.
Area of Science:
- Cardiology
- Immunology
- Biochemistry
Background:
- Acute coronary syndromes (ACS) trigger significant inflammation and leukocyte activation.
- The origin of this inflammation (local coronary vs. systemic) is debated.
- Inflammation is linked to poor prognosis in ACS.
Purpose of the Study:
- To investigate the source of inflammation in ACS.
- To measure markers of leukocyte and endothelial activation in ACS patients.
Main Methods:
- Measured soluble cell adhesion molecules (sICAM-1, sVCAM-1) and monocyte ligands (CD11b, CD49d) in 21 ACS patients.
- Used ELISA for soluble molecules and flow cytometry for cell surface expression.
Main Results:
- ACS patients showed significantly higher levels of monocyte receptor CD11b and soluble intercellular adhesion molecule-1 compared to controls.
- Elevated levels of CD11b (531 vs. 345 MFI) and sICAM-1 (329 vs. 232 ng/ml) were observed.
Conclusions:
- Found reciprocal activation of monocyte ligands and endothelial adhesion molecules in ACS patients.
- Suggests a systemic inflammatory upregulation involving both leukocytes and endothelium.
- Indicates a systemic, rather than local, source of inflammation in acute coronary disease.
Background:
The acute coronary syndromes are associated with an intense inflammatory response and sustained leukocyte activation. This inflammatory state has been correlated with an adverse prognosis, but the source of this inflammation remains controversial, with evidence that it may arise either from the coronary vasculature or from the systemic endothelium.
Methods:
Levels of soluble cell adhesion molecules, and of their respective monocyte cell surface ligands, were measured in the peripheral serum of 21 patients presenting with acute coronary syndromes. Soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1 were measured by enzyme linked immunosorbent assay and expression of the monocyte integrins CD11b (Mac-1) and CD49d (VLA-4) was measured by direct immunofluorescence using flow cytometry.
Results:
High levels of the monocyte receptor CD11b (531 vs. 345 MFI, P<0.01), and its soluble intercellular adhesion molecule-1 (329 vs. 232 ng/ml, P<0.01), were noted in patients with acute coronary syndromes compared to healthy controls.
Conclusions:
Reciprocal activation of monocyte receptor ligands and endothelial adhesion molecules was found in the peripheral blood of patients with acute coronary syndromes. This may indicate a coordinated state of pro-inflammatory upregulation with widespread activation of both leukocytes and endothelium and suggests a systemic rather than local source for inflammation in acute coronary disease.