Fig. 9.
Fig. 9. Inhibition of neutrophil binding to endothelial cells by LXA4 analogs (A) or by anti–E-selectin, anti–L-selectin, and anti-CD18 MoAbs and 15-R/S-methyl-LXA4 (B). Confluent HCAEC monolayers were cultured with 1 μg/mL LPS with or without LXA4 analogs for 6 hours at 37°C. (A) Neutrophils were preincubated for 30 minutes with LXA4 analogs or medium as indicated before addition to activated HCAEC. Values are the means ± SEM of 3 to 6 experiments using neutrophils from different donors. *P < .05 v LPS-treated HCAEC. (B) Neutrophils were treated with 15-R/S-methyl-LXA4 (5 μmol/L) or the indicated MoAbs before and during the assay. Neutrophil adhesion to unstimulated HCAEC was 0.41 ± 0.03 × 104 cells per well. The irrelevant MoAb MOPC-21 (IgG1) was used as a negative control. The results represent the mean ± SEM of 5 experiments using neutrophils from different donors.

Inhibition of neutrophil binding to endothelial cells by LXA4 analogs (A) or by anti–E-selectin, anti–L-selectin, and anti-CD18 MoAbs and 15-R/S-methyl-LXA4 (B). Confluent HCAEC monolayers were cultured with 1 μg/mL LPS with or without LXA4 analogs for 6 hours at 37°C. (A) Neutrophils were preincubated for 30 minutes with LXA4 analogs or medium as indicated before addition to activated HCAEC. Values are the means ± SEM of 3 to 6 experiments using neutrophils from different donors. *P < .05 v LPS-treated HCAEC. (B) Neutrophils were treated with 15-R/S-methyl-LXA4 (5 μmol/L) or the indicated MoAbs before and during the assay. Neutrophil adhesion to unstimulated HCAEC was 0.41 ± 0.03 × 104 cells per well. The irrelevant MoAb MOPC-21 (IgG1) was used as a negative control. The results represent the mean ± SEM of 5 experiments using neutrophils from different donors.

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