GM-CSF reverses the defects in phagocytosis induced by rhC5a. (A) Addition of GM-CSF restores effective phagocytosis of opsonized zymosan in neutrophils exposed to C5a. P < .0001 by Kruskal-Wallis; **P < .01, ***P < .001 by Dunn posthoc test. Data are displayed as median and interquartile range (n = 10 healthy donors). (B) Addition of GM-CSF restores RhoA activation in neutrophils treated with rhC5a and exposed to opsonized zymosan. **P = .007 by Mann-Whitney U test. Data are displayed as median and interquartile range (n = 10 healthy donors). Note: C5a data are the same as those presented in Figure 1A, and the GM-CSF data are shown separately for reasons of clarity—separation does not alter the statistical significance of the differences noted. (C) Addition of GM-CSF restores actin polymerization in neutrophils treated with rhC5a and exposed to opsonized zymosan. P = .0001 for differences between treatments by 2-way ANOVA, **P < .01 by Bonferroni posthoc test for differences between treatments. Data are shown as mean and SEM (n = 8 healthy donors). (D) Addition of PI3Kδ inhibitor IC87114 after 30 minutes of treatment with C5a fails to resurrect phagocytosis. P = .009 by Kruskal-Wallis, *P < .05 by Dunn posthoc test. Data are displayed as median and interquartile range (n = 5 healthy donors).