Figure 4
Figure 4. Expression of IL-8 with E-selectin allows mAb RMAC8-enhanced adhesion to ECs. (A) the ability of adIL-8 is shown at increasing MOI to stimulate PMN arrest on HMEC-1 cells coinfected with E-selectin (100 MOI), when assayed at 1.5 dynes/cm2 (*P < .03, **P < .01). (B) adIL-8 (100 MOI) synergized with mAb RMAC8 is shown to increase adhesion (at 1.5 dynes/cm2) to HMEC-1 cells coinfected with E-selectin (100 MOI) and that this was inhibited by anti–CXCR-1 and/or -2 (*P < .05 compared with no adIL8; **P < .04 compared with adIL-8 but no RMAC8; #P < .03, †P < .05 compared with adhesion in the absence of blocking antibody). (C) PMN adhesion to RMAC8-coated TNFα-activated HMEC-1 cells was inhibited by anti-CXCR-1 and -2 (*P < .001). All values are mean + SEM of 3 experiments.

Expression of IL-8 with E-selectin allows mAb RMAC8-enhanced adhesion to ECs. (A) the ability of adIL-8 is shown at increasing MOI to stimulate PMN arrest on HMEC-1 cells coinfected with E-selectin (100 MOI), when assayed at 1.5 dynes/cm2 (*P < .03, **P < .01). (B) adIL-8 (100 MOI) synergized with mAb RMAC8 is shown to increase adhesion (at 1.5 dynes/cm2) to HMEC-1 cells coinfected with E-selectin (100 MOI) and that this was inhibited by anti–CXCR-1 and/or -2 (*P < .05 compared with no adIL8; **P < .04 compared with adIL-8 but no RMAC8; #P < .03, †P < .05 compared with adhesion in the absence of blocking antibody). (C) PMN adhesion to RMAC8-coated TNFα-activated HMEC-1 cells was inhibited by anti-CXCR-1 and -2 (*P < .001). All values are mean + SEM of 3 experiments.

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