Figure 4
Caspase-8-mediated IL-1 signaling is crucial for OVA-induced allergic pulmonary inflammation. (a) The expression of Il1a and Il1b in lung tissue from OVA-treated Rip3−/− and Rip3−/−Casp8−/− mice were analyzed by qRT-PCR. (b) WT and IL-1R mutant mice (Il1r−/−) were sensitized with OVA/alum and challenged with OVA. Fluorescence-activated cell sorting analysis was performed for pulmonary immune cell infiltration 24 h after the last OVA challenge. (c) Representative lung hematoxylin and eosin sections from OVA-treated WT and Il1r−/− mice (left), and clinical scores of pulmonary disease on the basis of inflammation, alveolar exudates, and vascular muscle hypertrophy (right). (d and e) Cytokines (d) and IgE (e) in the supernatants of the lungs collected from OVA/alum-sensitized and OVA-challenged (OVA), or PBS-treated WT and Il1r−/− mice. (f and g) IL-1α (f) and IL-1β (g) in the supernatants of the lungs collected from OVA/alum-sensitized and OVA-challenged (OVA) WT, Rip3−/−, Rip3−/−Casp8−/− (R3/C8−/−), Rip3−/−Fadd−/− (F3/Fa−/−), Caspase-1/11−/− (C1/11−/−), Elastase−/−, Nepr3−/−, and Ctsg−/− mice or PBS-treated WT mice. Arrow and arrowhead indicate immune cell infiltration and thick airway muscle, respectively. Data represent mean±s.e.m. Results are representative of three independent experiments. *P<0.05; **P<0.01; ***P<0.001; ****P<0.0001; IL, interleukin; NS, not significant; PBS, phosphate-buffered saline; OVA, ovalbumin; WT, wild type.
