Figure 3
From: Platelet activation and prothrombotic properties in a mouse model of peritoneal sepsis
Expression of surface platelet activation markers and elevation of leukocyte-platelets interactions during sepsis. (a) Expression of the surface platelet activation marker CD62P analyzed by flow cytometry during sepsis. (b) Activation of αIIbβ3 (GpIIbIIIa) integrin at the platelet surface assessed by oregon green fibrinogen binding and flow cytometry analysis. Results are expressed as median fluorescence intensity and are median fold increase ± IQR of 6 to 8 independent experiments (*p < 0.05, **p < 0.01). (c) Whole blood monocyte-platelet aggregates quantified at different times post surgery in sham and CLP-operated mice. Results are expressed as percentage of monocyte-platelet aggregates and are median ± IQR of 4 to 6 independent experiments (*p < 0.05, **p < 0.01, ***p < 0.001). (d) Density of platelets per monocytes. The MFI values of the platelet marker (CD41) on monocytes was measured 24 h after CLP by flow cytometry to evaluate the platelet density per monocyte (left panel). After sorting by flow cytometry the platelet-monocyte aggregates were spin down onto poly-lysine coated slides and observed by confocal microscopy (right panel). A representative confocal image is show to illustrate the interaction of platelets (CD41, green) and monocyte (CD115, red) 24 h post CLP. The monocyte nucleus was labeled with DAPI (blue). (e) Whole blood neutrophil-platelet aggregates quantified at different times after surgery in sham and CLP-operated mice. Results are expressed as percentage of neutrophil-platelet aggregates and are median ± IQR of 3 to 7 independent experiments (*p < 0.05) (left panel). The MFI values of the platelet marker (CD41) on neutrophils was measured 48 h after CLP to evaluate the platelet density per neutrophil (right panel).
