Fig. 1.
Fig. 1. Distribution of CXCR1 expression on IL-8–, LPS-, and TNF-–treated neutrophils. Purified peripheral blood PMNs were incubated for 1 hour at 37°C in media alone (RPMI/10% fetal calf serum) or stimulated with IL-8 (500 ng/mL), LPS (100 ng/mL), or TNF- (50 ng/mL). Cells were then stained with FITC-conjugated Ab to CXCR1 and examined by confocal microscopy using an oil immersion lens at 600× magnification. (A) Cellular distribution of maximal CXCR1 fluorescence for each treatment is shown at left, and transmission light microscopy of the same cell is shown at right, with size bars representing 10 μm. (B) Mean membrane v cytoplasm CXCR1 staining intensity is plotted for n = 15 (±SEM) cells per treatment group. *Statistical significance (P < .05) using 1-way ANOVA for membrane luminosity of control untreated groupv treated groups. **Statistically significant increase (P < .05; one-way ANOVA) in cytoplasm luminosity vmembrane luminosity of IL-8–treated cells.

Distribution of CXCR1 expression on IL-8–, LPS-, and TNF-–treated neutrophils. Purified peripheral blood PMNs were incubated for 1 hour at 37°C in media alone (RPMI/10% fetal calf serum) or stimulated with IL-8 (500 ng/mL), LPS (100 ng/mL), or TNF- (50 ng/mL). Cells were then stained with FITC-conjugated Ab to CXCR1 and examined by confocal microscopy using an oil immersion lens at 600× magnification. (A) Cellular distribution of maximal CXCR1 fluorescence for each treatment is shown at left, and transmission light microscopy of the same cell is shown at right, with size bars representing 10 μm. (B) Mean membrane v cytoplasm CXCR1 staining intensity is plotted for n = 15 (±SEM) cells per treatment group. *Statistical significance (P < .05) using 1-way ANOVA for membrane luminosity of control untreated groupv treated groups. **Statistically significant increase (P < .05; one-way ANOVA) in cytoplasm luminosity vmembrane luminosity of IL-8–treated cells.

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