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Figure 1 | BMC Immunology

Figure 1

From: Bone marrow cell derived arginase I is the major source of allergen-induced lung arginase but is not required for airway hyperresponsiveness, remodeling and lung inflammatory responses in mice

Figure 1

Characterization of arginase I-deficient BM chimeric mice. In A, OVA-specific IgG1 was measured in plasma. Representative experiment (2–4 mice per group) of 3 experiments performed is shown. In B, Northern blot analysis for arginase I in allergen-challenged (OVA- ovalbumin model and Asp- Aspergillus fumigatus model) wild type and arginase I-deficient BM chimeras is shown. Ethidium bromide-stained gel is shown as loading control. In C, in situ hybridization with arginase I anti-sense probe is shown. Panels (a) and (b) are from an allergen-challenged arginase I +/- BM chimeric mouse and (c) and (d) are from an allergen-challenged arginase I -/- BM chimeric mouse. (a) and (c) are dark-field and (b) and (d) are bright-field images of the same area. Representative micrographs of 3 mice in each group are shown. In D and E, arginase activity on lung homogenates is shown. Representative of 4 experiments (2 with OVA and 2 with Asp) for arginase I chimeras, and 3 for arginase II-deficient mice are shown. Data are from 2–6 mice per group in the individual experiment with 7–15 total mice per group. For both arginase I chimeras and arginase II-deficient mice, two-way ANOVA demonstrated a statistically significant (P < 0.01) effect of treatment (allergen compared to saline), with no statistically significant effect of interaction (P > 0.05). The P value for the effect of genotype was P = 0.055 in arginase I BM chimeras and P = 0.98 in arginase II-deficient mice.

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BMC Immunology

ISSN: 1471-2172

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