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. 2011 Jan 5;6(1):e15943. doi: 10.1371/journal.pone.0015943

Figure 6. Dectin-1- or MyD88-deficiency in alveolar macrophages does not affect Arginase1 expression but impairs fungal clearance.

Figure 6

(A) WT, Dectin-1-/- and MyD88-/- mice were infected with 10×106 RC and CD11c+ cells were isolated by BAL at 48 hours p.i. Quantitative RT-PCR was performed to measure Arg1 mRNA expression in CD11c+ cells from infected WT, Dectin-1-/- and MyD88-/- and the fold increase shown are relative to that in CD11c+ cells from uninfected group. Values shown are mean±SEM (B) Fungal burden expressed as CFU per lung was measured in lungs harvested from WT, Dectin-1-/- and MyD88-/- mice at 48 hours p.i. Values shown are mean±SEM. Data shown are representative of two independent experiments (n = 6-8 mice in each group). (C) Phagocytosis of FITC-labeled A. fumigatus conidia by CD11c+ alveolar macrophages as examined by confocal microscopy. Images show overlay of FITC (green for conidia) and Hoechst stain (blue for nuclei) and Cell tracker (red for cell cytoplasm). The upper panel shows images captured at 60X in single optical plane and the lower panel shows 3X digital zoom images. Quantification of conidia present intracellularly was done using Metamorph and results are expressed as percentage of cells with FITC-conidia. Labeled conidia were easily identified in the macrophages isolated from both WT and MyD88-deficient mice but were rare in cells isolated from Dectin-1-/- mice.