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Upregulation of the CD40/CD40 ligand dyad and platelet-monocyte aggregation in cigarette smokers
S A Harding1, J Sarma, D H Josephs
1Centre for Cardiovascular Sciences, Royal Infirmary of Edinburgh, Edinburgh, United Kingdom.
Insights
Cigarette smoking increases markers of inflammation and blood clot formation, specifically the CD40/CD40 ligand (CD40L) pathway and platelet-monocyte aggregation. These changes may explain smoking
Area of Science:
- Cardiovascular Research
- Immunology
- Hematology
Background:
- Smoking is a significant risk factor for cardiovascular disease, linked to inflammation and thrombosis.
- The CD40/CD40 ligand (CD40L) pathway and platelet-monocyte aggregation are implicated in atherothrombosis.
Purpose of the Study:
- To investigate alterations in the CD40/CD40L dyad expression and platelet-monocyte aggregation in cigarette smokers.
Main Methods:
- Compared C-reactive protein (CRP), soluble CD40L (sCD40L), and surface expression of CD40/CD40L and platelet-monocyte aggregates in 25 smokers and 25 non-smokers.
- Measured plasma cotinine levels to assess smoking exposure.
Main Results:
- Smokers exhibited significantly higher serum CRP levels (P=0.008).
- Elevated surface expression of CD40 on monocytes (P=0.006), CD40L on platelets (P=0.03), and platelet-monocyte aggregates (P=0.02) were observed in smokers.
- Plasma cotinine levels correlated with increased monocyte CD40, platelet CD40L, and platelet-monocyte aggregates.
Conclusions:
- Cigarette smokers demonstrate an upregulation of the CD40/CD40L dyad and enhanced platelet-monocyte aggregation.
- These molecular changes may contribute to the atherothrombotic effects associated with smoking.
Background:
Smoking is a potent cardiovascular risk factor and is associated with proinflammatory and prothrombotic responses. The CD40/CD40 ligand (CD40L) dyad and platelet-monocyte aggregation mediate a range of proinflammatory and prothrombotic processes thought to be important in atherothrombosis. We investigated whether expression of the CD40/CD40L dyad and platelet-monocyte aggregation are altered in cigarette smokers.
Methods And Results:
C-reactive protein (CRP), soluble (s) CD40L, and surface expression of CD40L on platelets and T cells and of CD40 on monocytes and platelet-monocyte aggregates were compared in 25 cigarette smokers and 25 age- and gender-matched nonsmokers. Cigarette smokers had increased serum CRP (2.47+/-2.60 versus 0.94+/-0.96 mg/L, P=0.008) and appeared to have elevated plasma sCD40L (0.8+/-1.09 versus 0.37+/-0.21 ng/mL, P=0.07) concentrations. Smokers also had increased surface expression of CD40 on monocytes (45.9+/-7.7% versus 39.9+/-6.5%, P=0.006), of CD40L on platelets (2.9+/-1.0% versus 2.3+/-0.6%, P=0.03), and of platelet-monocyte aggregates (26.6+/-10.9% versus 19.7+/-8.6%, P=0.02). Plasma cotinine concentrations correlated with monocyte CD40 expression, platelet CD40L expression, and platelet-monocyte aggregates.
Conclusions:
Cigarette smokers have upregulation of the CD40/CD40L dyad and platelet-monocyte aggregation that may account for the atherothrombotic consequences of this major cardiovascular risk factor.
