FcγR-mediated phagocytosis by alveolar macrophages (AMs) is regulated by GM-CSF in the lungs and expression of PU.1 in AMs.

(A-C) Primary AMs were recovered by BAL from mice in which GM-CSF expression was normal (GM^+/+), absent (GM^−/−), or present only in the lungs (SPC-GM^+/+/GM^−/−) and challenged with unopsonized beads (Beads alone) or IgG-opsonized beads (Beads + Ab) as described in “Materials and methods.” Phagocytic indices are shown. Data represent means ± SEM; n = 4 (GM^−/−and SPC-GM^+/+/GM^−/−) or n = 3 (GM^−/−) mice per group; AMs from each mouse were analyzed individually. Differences in phagocytic indices for FcγR-mediated and non-FcγR–mediated phagocytosis (Beads + Ab, Beads alone, respectively) by AMs from GM^+/+ and SPC-GM^+/+/GM^−/− were significant (P < .01). Corresponding phagocytic indices for AMs from GM^−/− mice were not significantly different (P = .86). (D-F) Cultured AM cell lines were challenged as above except that plates of cells were also challenged in the presence of FcγR-blocking antibody (Beads + Ab +Fc block). Phagocytic indices are shown. Data represent means ± SEM; n = 4 determinations per group. Differences in phagocytic indices for FcγR-mediated and non-FcγR–mediated phagocytosis (Beads + Ab, Beads alone, respectively) in MH-S and mAM$PU.1+$ cells were significant (P < .0001). FcγR-mediated phagocytosis was completely blocked by addition of anti-FcγR antibody. Phagocytosis was not detected in mAM$GFP+$ cells (*).