Neutrophil slow rolling and arrest in vivo. (A) Dual bright field and fluorescence imaging of rolling neutrophils in postcapillary venules of the mouse cremaster muscle. (B-C) Rolling velocities of neutrophils after TNF-α pretreatment of the mouse cremaster muscle in (B) Tln1^fl/flMx1-Cre/LysM^GFP and (C) Fermt3^−/−/LysM^GFP mixed chimeric mice. All mice received an intravenous injection of an anti–P-selectin mAb (clone RB40.34, 30 μg/mouse) at least 15 minutes before image acquisition. A blocking anti–LFA-1 mAb (30 μg/mouse) was injected to determine the dependence of rolling velocity on LFA-1. Data are presented as cumulative velocity histograms and as mean rolling velocities ± SEM (n = 3 mice each). (D) Arrested neutrophils were counted after intravenous injection of CXCL1 (600 ng). Data are mean ± SEM (number of arrested cells per unit area of the blood vessel wall; n = 3 mice each), normalized according to the ratio of circulating wild-type to gene-deficient neutrophils before CXCL1 injection. (E) Neutrophil influx into the peritoneal cavity was measured 8 hours after 1 mL intraperitoneal injection of 4% thioglycollate medium. Data are mean ± SEM (number of neutrophils in the peritoneal lavage; n = 3 mice), normalized according to the ratio of circulating wild-type (GFP⁺) to gene-deficient (GFP⁻) neutrophils before thioglycollate injection.