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. 2016 Sep 19;213(10):1999–2018. doi: 10.1084/jem.20160393

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© 2016 Bajrami et al.

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Figure 1. — Rapid neutrophil mobilization in early-stage acute inflammation is mainly mediated by CXCR2 ligands. (A) Neutrophil counts in PB after E. coli administration in the peritonitis model. Changes of PB neutrophil count over time were analyzed by one-way ANOVA–repeated measures. The control group was time 0. (B) The speed of neutrophil count changes at each indicated time period was quantified. The control group was −30 to 0 min. (C) The concentrations of CXCR2 ligand MIP-2 in blood serum. (D) The concentrations of CXCR2 ligand KC in blood serum. The control group was time 0 for each group. Differences over time between groups were analyzed using multivariate ANOVA with measures repeated over time. E.coli treatment significantly (P < 0.01) increased serum MIP-2 and KC levels. (A–D) Dunnett's multiple comparison test versus the control group was used. (E) CXCR2 blockade suppresses rapid neutrophil mobilization during early-stage acute inflammation. CXCR2 antibodies or IgG (as control) was i.v. administered to each mouse. (F) CXCR2 ligand MIP-2 induces rapid neutrophil mobilization. MIP-2 (1 µg in 100 µl PBS) and/or CXCR2 antibodies (2 µg in 100 µl PBS) were i.v. administered. (E and F) Student’s t test versus control (mice treated with IgG) was used. All data are means ± SD of three experiments (n = 6 mice). *, P < 0.01. Ab, antibody.