Fig. 3: Depletion of mitochondrial H2O2 abolishes low-dose HDM-induced airway tolerance with induction of allergic airway inflammation. | Mucosal Immunology

Fig. 3: Depletion of mitochondrial H2O2 abolishes low-dose HDM-induced airway tolerance with induction of allergic airway inflammation.

From: Early life exposure to house dust mite allergen prevents experimental allergic asthma requiring mitochondrial H2O2

Fig. 3

Analysis of lung tissue isolated from MCAT or WT littermate mice sensitized with low-dose HDM (0.5 µg, referred to here as Tol) at 2 weeks of age, followed by challenges with 25 µg HDM at 6 weeks of age. Mice were sacrificed 24 h after the last challenge. Mice without HDM pre-sensitization at 2 weeks (PBS exposure) but only subjected to HDM challenges at 6 weeks were considered as inflammation group (referred to here as Infl) while those without any exposure were considered as naïve controls. a, b PAS staining of lung sections showing cellular infiltration around blood vessels and airways (black arrow) and mucus productions in the small airways (red arrow). Scale bar: 100 µm. Data shown in (a) are representative results and in (b) are median ± IQR summarized from three independent experiments with 6–12 mice per group. c Frequency and absolute number of the inflammatory cells based on analysis of BAL fluid. d Assay of total serum IgE levels. Data shown are median ± IQR combined from two independent experiments with 5–10 mice per group. e Assessment of airway hyperresponsiveness (AHR) in mice. Rn Newtonian resistance. MCh methacholine. Data shown in (c) are median ± IQR and in (e) are mean ± SEM combined from three independent experiments with 6–10 mice per group. Kruskal–Wallis with Dunn’s post hoc test for multiple comparisons (b, c, d). Two-way ANOVA with Tukey’s multiple comparisons test (e). *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001; nsP > 0.05.

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