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. 2016 Aug 2;4(3):350–361. doi: 10.1002/iid3.118

Figure 1.

Figure 1

LXR‐deficient mice display reduced airway inflammation, airway hyper‐reactivity (AHR) and goblet cell hyperplasia in OVA‐induced asthma as compared to wild‐type (WT) mice. WT, LXRα−/−, LXRβ−/−, and LXRα−/−β−/− mice were sensitized against OVA and subsequently challenged with aerosolized OVA. (A) Differential cell counts in the bronchoalveolar lavage (BAL) after exposure to six OVA aerosols measured by flow cytometry. (B) Eosinophils and CD4+ T cells in the BAL assessed by flow cytometry after 2–8 consecutive OVA aerosols. (C) Dynamic airway resistance [R], elastance [E], and compliance [C] was determined in mice exposed to increasing doses of methacholine after exposure to six OVA aerosols. (D) Mucus production evaluated by PAS staining of lung paraffin sections of mice exposed to six OVA aerosols. (E) OVA‐specific IgE titer in serum and bronchoalveolar lavage fluid measured by ELISA. (A) A Kruskal–Wallis test followed by a post hoc Dunn's test was used. (B, D, and E) Statistical analysis between two groups was performed using a Mann–Whitney U test. Data are shown as mean ± SD, n = 5 to 7 mice per group. The results show one representative experiment out of at least two independent experiments. (C) The repeated measures in dynamic AHR of three independent experiments were analyzed by residual maximum likelihood. Data are shown as mean ± SE, n = 5–7 mice per group. Significant P‐values were ranked as P < 0.05 (*), P < 0.01 (**), and P < 0.001 (***).