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Upregulation of platelet CD40, CD40 ligand (CD40L) and P-Selectin expression in cigarette smokers: a flow cytometry
Horst Neubauer1, Patricia Setiadi, Antonio Pinto
1Cardiovascular Center, Ruhr University Bochum, Germany. horst.neubauer@rub.de
Insights
Cigarette smoking significantly elevates markers of platelet activation and inflammation in healthy individuals. This research highlights how smoking promotes a pro-inflammatory and pro-thrombotic state, contributing to cardiovascular disease.
Area of Science:
- Cardiovascular Science
- Hematology
- Immunology
Background:
- Cigarette smoking is a major risk factor for cardiovascular disease (CVD) and mortality.
- Smoking is associated with inflammation, platelet activation, and atherosclerosis.
- The impact of smoking on platelet proinflammatory markers requires further investigation.
Purpose of the Study:
- To investigate platelet activation and expression of proinflammatory markers in smokers.
- To quantify P-selectin (CD62P) and CD40/CD40L expression on platelets from smokers and controls.
Main Methods:
- Flow cytometry was used to measure platelet activation markers.
- Platelet-rich plasma was obtained from 34 healthy volunteers (19 smokers, 15 controls).
- Basal and stimulated (ADP, TRAP) expression of CD62P, CD40, and CD40L were evaluated.
Main Results:
- Smokers showed significantly higher basal levels of platelet-bound CD40, CD40L, and P-selectin compared to controls.
- Stimulation with ADP or TRAP resulted in higher marker values in smokers, though not statistically significant.
- These findings indicate cigarette smoking activates platelets and the CD40-CD40L pathway.
Conclusions:
- Cigarette smoking induces platelet activation and a proinflammatory state in healthy individuals.
- The study demonstrates smoking's role in promoting a prothrombotic condition.
- These effects contribute to accelerated atherosclerosis and increased cardiovascular risk.
Abstract:
Cigarette smoking is a well known risk factor for cardiovascular disease with a great impact on mortality. Studies have linked smoking to inflammation, platelet activation and enhanced atherosclerosis. The present study investigated the activation and expression of proinflammatory markers on platelets obtained from smokers. The expression of P-selectin (CD62P) (as a marker of activation) and CD40/CD40L (as a marker for proinflammatory processes) were quantified in platelets by flow cytometry. Platelet-rich plasma was obtained from 34 apparent healthy volunteers (19 cigarette smokers, 15 age-matched control persons). Basal measurements and the response to stimulation with ADP and TRAP (10, 30, 100 micromol/l) were evaluated. Values given (mean fluorescence index, MFI) are mean +/- standard deviation. The basal values of platelet bound CD40 (3.20 +/- 0.50 vs. 2.71 +/- 0.28; P = 0.002), CD40L (1.10 +/- 0.12 vs. 0.95 +/- 0.12; P = 0.005) and P-selectin (0.70 +/- 0.21 vs. 0.55 +/- 0.11; P = 0.012) were significantly elevated in smokers as compared to controls. In addition, higher values were noted on stimulation with ADP or TRAP in smokers, although these different values were without statistical significance. According to our data cigarette smoking activates platelets (P-selectin expression) and stimulates the CD40-CD40L-pathway in otherwise healthy volunteers. These findings emphasize that cigarette smoking leads to a proinflammatory and prothrombotic state thus contributing to accelerated atherosclerosis.
