Fig. 4.

Hyperoxic exposure induces alveolar monocyte/macrophage infiltration into neonatal lungs that is ameliorated by CO-induced treatment. Representative flow cytometric scattergrams of monocyte/macrophage subpopulations within the lungs of wild-type (WT) and HO-1-null mice exposed to normoxia and hyperoxia for 14 days. Wild-type mice were also exposed to normoxia + CO or hyperoxia + CO. Each dot plot is representative of 4 independent experiments. A: CD45+, CD11c+, F4/80+ macrophages. B: gating scheme used in subsequent flow cytometric analysis. C: whole lung live CD45+ cells were analyzed for expression of CD11c and CD11b. D–F: comparison of cell counts for F4/80 and CD11c double-positive macrophages (D), CD11c^high CD11b^high exudative macrophages (subpopulation B, E), and CD11c^lowCD11b^high inflammatory monocytes (subpopulation C, F). Cell counts represent the number of cells per 10⁶ events. Hyperoxia increased the trafficking of macrophage subpopulations into the neonatal lung, and CO treatment attenuated macrophage recruitment. HO-1^−/− mice showed increases lung macrophages. n = 4–10 per group, means ± SE, *compared to hyperoxia alone, P < 0.05, ANOVA.