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Effects of alimentary lipemia and inflammation on platelet CD40-ligand
Thorsten Kälsch1, Elif Elmas, Xuan Duc Nguyen
11st Department of Medicine, University Hospital Mannheim, Medical Faculty Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany.
Insights
Acute lipemia after a fatty meal decreases CD40-ligand (CD40L) expression on platelets and soluble CD40L plasma levels. This suggests increased CD40L system turnover, impacting atherosclerosis progression.
Area of Science:
- Cardiovascular Biology
- Immunology
- Metabolic Research
Background:
- The CD40-CD40L pathway is implicated in atherosclerosis development, particularly in hypercholesterolemia.
- Understanding the impact of postprandial lipemia and inflammation on this pathway is crucial.
Purpose of the Study:
- To investigate the effects of acute postprandial lipemia and inflammatory stimulation on platelet and monocyte activation.
- To assess changes in CD40-ligand (CD40L) expression and plasma levels.
Main Methods:
- Healthy subjects (n=31) consumed a fatty meal.
- Blood samples were analyzed pre- and post-meal, with and without lipopolysaccharide (LPS) stimulation.
- Flow cytometry measured CD40L, CD62P expression, tissue factor, and platelet-monocyte aggregates.
- Soluble CD40L plasma levels were quantified via ELISA.
Main Results:
- Postprandial lipemia significantly decreased platelet CD40L and CD62P expression and plasma soluble CD40L.
- No significant changes in monocyte tissue factor or platelet-monocyte aggregates were observed post-meal.
- LPS stimulation increased platelet-monocyte aggregates post-meal but did not alter CD40L or CD62P expression.
Conclusions:
- Acute alimentary lipemia reduces CD40L expression on platelets and in plasma.
- These findings suggest an accelerated turnover within the CD40L system following a fatty meal.
- The interplay between lipemia, inflammation, and CD40L signaling warrants further investigation in cardiovascular disease.
Introduction:
In patients with chronic hypercholesterolemia, the CD40-CD40L dyad is upregulated, contributing to the initiation and progression of atherosclerosis. Our aim was to describe the role of postprandial lipemia and inflammatory stimulation on platelet and monocyte activation and CD40-ligand (CD40L) levels.
Methods And Results:
Before and 2 h after consumption of a defined fatty meal, whole blood samples of 31 healthy subjects were incubated with endotoxin (LPS). CD40-ligand and CD62P expression on platelets, tissue-factor expression on monocytes and platelet-monocyte aggregates were measured with flow cytometry. Soluble CD40-ligand plasma levels were measured with an ELISA. After the meal, serum triglyceride levels increased from 137.6+/-60.5 mg/dl to 201.5+/-75.0 mg/dl. Expression of CD40L and CD62P on platelets and plasma levels of soluble CD40L were significantly decreased. No significant changes after the meal were observed concerning tissue factor expression on monocytes and platelet-monocyte aggregates. Addition of LPS showed no significant effect concerning CD40L or CD62P expression on platelets, whereas the amount of platelet-monocyte aggregates significantly increased under LPS stimulation after the fatty meal.
Conclusions:
Acute alimenatry lipemia leads to a decreased expression of CD40L on platelets and a reduced plasma level of sCD40L, suggesting an increased turnover in the CD40L system.
Condensed Abstract:
Before and after a fatty meal, blood samples of 31 healthy subjects were incubated with LPS. After the meal, expression of CD40L and CD62P on platelets and plasma levels of soluble CD40L were significantly decreased. Addition of LPS showed no effect concerning CD40L or CD62P expression, whereas the amount of platelet-monocyte aggregates significantly increased under LPS stimulation after the fatty meal.
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