FIGURE 2.

Lipoxin A₄ receptor, FPR2/ALX, expression on neutrophils from patients with atherosclerosis versus healthy controls. Whole blood from healthy controls (n = 5) or patients with atherosclerosis (n = 5) was exposed to inflammatory stimulus, either in the absence or presence of lipoxin A₄ (LXA₄: 500 nM) or lipoxin B₄ (LXB₄: 500 nM). The neutrophil surface expression of FPR2/ALX was measured by flow cytometry. (A) Neutrophil FPR2/ALX expressions were measured as % positive cells (left panel) and cellular mean fluorescence intensity (MFI) (right panel). The expression was measured in controls (white bars) and patients (gray bars). The cells were untreated (Unstim.) or stimulated with chemotactic peptide N‐formyl‐Met‐Leu‐Phe (fMLP, 0.4 μM). Representative histograms for the MFI of respective receptor expression and indicated conditions are shown for controls (dashed line) and patients (solid line), where the gates were determined using a negative population (gray shaded peaks). (B) LXA₄ (blue bars) and LXB₄ (green bars)‐induced changes to FPR2/ALX expression was calculated as the log₂ fold change relative to respective vehicle‐treated condition. The samples were stimulated as indicated. The bar graphs show levels as % marker positive cells (left panel) and MFI of indicated markers (right panel). Representative MFI histograms for each receptor expression under respective treatment conditions are shown for vehicle (black line), LXA₄ (blue line) and LXB₄ (green line), where the gates were determined using a negative population (gray shaded peaks). Assuming non‐Gaussian distribution of the human samples, statistical analysis was determined using Mann–Whitney U test when comparing two groups, and Kruskal–Wallis test with Dunn's post hoc comparisons when comparing more than two groups. Data are presented as mean ± standard error of the mean (SEM). Statistical significance is indicated as *p < .05, **p < .01, ***p < .001