Figure 2. Lack of dietary aryl hydrocarbon receptor (AhR) ligands does not impact airway allergic type 2 inflammation.

Mice were placed on AhR-poor or indole-3-carbinol (I3C) diet for 3 wk of adaptation prior to the start of experiments. Mice were exposed to papain or vehicle (PBS) intranasally four times at days 0, 1, 13, and 20. (A–D) 24 hr after the last exposure, tissues were analyzed. (A) Cell counts in bronchoalveolar lavage. (B) Cytokine concentration in bronchoalveolar lavage. (C) Normalized numbers of lymph nodes T cells were restimulated ex vivo, and cytokine secretion was measured in the supernatant after 24 hr. LN = lymph nodes. (D) Lung lysates were analyzed by RT-qPCR. (E) Blood was collected at day 20 and IgE concentration measured in the serum. For all panels, median is shown (n = 8 in two independent experiments). Kruskal–Wallis test. *p<0.05; **p<0.01; ***p<0.001.

Figure 2—figure supplement 1. Gating strategy for bronchoalveolar cells.

Bronchoalveolar cells were gated on live singlets. One representative example for mice treated with vehicle (A) or papain (B).