Coro1A controls PMN adhesion under flow conditions by regulating LFA-1 affinity. (A) Induction of adhesion of Coro1A^+/+ and Coro1A^−/− PMNs under flow conditions (1 dyne/cm²) in microflow chambers coated with immobilized rmP-selectin, rmICAM-1, and rmCXCL1 at indicated times (n = 5). *P < .05; **P < .001 versus Coro1A^−/− PMNs; #P < .05 versus initially adherent Coro1A^+/+ PMNs at 1 minute. Mean ± standard deviation. (B) Induction of PMN adhesion in the presence of LFA-1 (clone M17/4, CD11a) or Mac-1 (clone M1/70, CD11b) function blocking or both, or control antibodies (IgG) under flow conditions (1 dyne/cm²). Relative adhesion of Coro1A^+/+ and Coro1A^−/− PMNs in percentage of all interacting PMNs (100%) after stimulation with rmCXCL1 for 9 minutes (n = 4). **P < .001. Mean ± standard deviation. (C) LFA-1 specific rmICAM-1 binding of Coro1A^+/+ and Coro1A^−/− PMNs stimulated for 3 minutes with 100 ng/mL of rmCXCL1, 10 μM of fMLP, 5 mM of Mn²⁺, or left unstimulated (minus sign). Mac-1 binding to rmICAM-1 was prevented by using a function blocking anti–Mac-1 antibody (clone M1/70). Fluorescence histograms (left) and quantitative analysis indicating percentage of cells positive for LFA-1 specific rmICAM-1-Fc binding in percentage of all PMNs (100%; middle), and median fluorescence intensity (right). Anti-LFA-1 antibody (clone M17/4, CD11a) was used to define negative control (n = 9, minus sign, unstimulated; n = 6, fMLP, rmCXCL1; n = 3, Mn²⁺). #P < .05; *P < .05 versus unstimulated control. Mean ± standard deviation. (D) CD11a cell surface expression of Coro1A^+/+ and Coro1A^−/− PMNs stimulated for 20 minutes with 100 ng/mL of rmCXCL1, 10 μM of fMLP, or left unstimulated (minus sign), isotype control (orange). Fluorescence histograms (left) and quantitative analysis (right) (n = 4). Mean ± standard deviation. n.s., not significant.