Figure 2.
Inflammatory mediators generated in severe COVID-19 contribute to platelet activation. (A-B) The percentage of P-selectin (CD62P) (A) and CD63 (B) expression on platelets was plotted against the concentration of fibrinogen in plasma. Linear regression and Spearman correlation were calculated according to the distribution of the dots. (C-D) Platelets from healthy volunteers were incubated with plasma from severe COVID-19 patients (severe, n = 16) or from SARS-CoV2− subjects (control, n = 11) for 2 hours. The percentages of P-selectin (C) and CD63 (D) are shown. All experiments were repeated with platelets from 3 independent healthy volunteers with similar results, and representative data from 1 of the platelet donors are shown. The horizontal lines in the box plots represent the median, the box edges represent the interquartile ranges, and the whiskers indicate the minimal and maximal value in each group. *P < .05 between selected groups.

Inflammatory mediators generated in severe COVID-19 contribute to platelet activation. (A-B) The percentage of P-selectin (CD62P) (A) and CD63 (B) expression on platelets was plotted against the concentration of fibrinogen in plasma. Linear regression and Spearman correlation were calculated according to the distribution of the dots. (C-D) Platelets from healthy volunteers were incubated with plasma from severe COVID-19 patients (severe, n = 16) or from SARS-CoV2 subjects (control, n = 11) for 2 hours. The percentages of P-selectin (C) and CD63 (D) are shown. All experiments were repeated with platelets from 3 independent healthy volunteers with similar results, and representative data from 1 of the platelet donors are shown. The horizontal lines in the box plots represent the median, the box edges represent the interquartile ranges, and the whiskers indicate the minimal and maximal value in each group. *P < .05 between selected groups.

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