A deficiency in endothelial p110γ impairs neutrophil accumulation on TNFα-stimulated CM venules. Rolling fraction (the number of GFP-expressing cells that attached and rolled on inflamed endothelium divided by the total flux of cells passing through the vessel) determined in mice (A) deficient in or chimeric for p110γ, (B) deficient in or chimeric for p110δ activity. ▪ indicates WT littermate (WT GFP^–/+); ▪, GFP^–/+p110γ^–/– or GFP^–/+p110δ^–/–; and ▨, p110γ^–/– or p110δ^–/– reconstituted with WT GFP^–/+ fetal liver cells. Results represent the mean plus or minus SD; *P < .05 as compared with WT littermates. n = number of mice/venules analyzed. Rolling velocities for consecutive interacting cells (n = 30 per venule) in mice (C) deficient in or chimeric for p110γ, or (D) deficient in or chimeric for p110δ. Data represent the mean ± SD for more than 150 cells per experimental condition; *P < .05. (E) Rolling fraction and (G) rolling velocities for p110γ^–/–/p110δ^–/– mice reconstituted with FLC from GFP^–/+ WT fetal liver cells (▪). ▪ indicates WT littermates reconstituted with GFP^–/+ WT fetal liver cells. *P < .05 as compared with controls. (F) Representative intravital micrographs depicting the extent of neutrophil adhesion to and transmigration across CM venules in WT mice (i) and p110γ^–/– (ii) or p110δ^–/– (iii) animals reconstituted with WT FLCs (3 hours after stimulation with TNFα).