Fig. 4: Clearance of endogenous bilirubin aggravates airway inflammation.
From: Bilirubin represents a negative regulator of ILC2 in allergic airway inflammation

a–f C57BL/6J mice were intranasally administered with PBS or papain 6 h after vehicle (Veh) or ZnPP (25 mg/kg) treatment for 5 days (n = 4–6 for each group). Mice were sacrificed 24 h after the last treatment. a Total bilirubin levels in plasma. b The frequencies and numbers of eosinophils in BAL were evaluated by flow cytometry. c The amounts of IL-5 and IL-13 in BAL were measured by ELISA. d Representative H&E staining of lung sections (bars, 100 μm) and the inflammation was determined by semi-quantitative scoring. e The proliferation of lung ILC2s was determined by Ki-67 staining. f The numbers of ILC2s and the frequencies of IL-5+IL-13+ ILC2s in lungs were determined by flow cytometry. g–k C57BL/6J mice were intranasally administered with papain or PBS 6 h after vehicle (Veh) or TCPOBOP (3 mg/kg) treatment for 5 days (n = 4–6 for each group). Mice were sacrificed 24 h after the last treatment. g The numbers of eosinophils in BAL were determined by flow cytometry. h The amounts of IL-5 and IL-13 in BAL were measured by ELISA. i Representative H&E staining of lung sections (bars, 100 μm) and the inflammation was determined by semi-quantitative scoring. j The absolute numbers of lung ILC2s and the frequencies of IL-5+IL-13+ILC2s in lungs were determined by flow cytometry. k The proliferation of lung ILC2s were determined by flow cytometry. Data are representative of three independent experiments, mean ± SEMs were shown. Unpaired Student’s t test was used. **p < 0.01, ***p < 0.001. Numbers within flow plots indicate the percentages of cells gated.