Figure 1
OVA-induced allergic pulmonary inflammation is significantly reduced in the absence of caspase-8 or FADD. (a) Wild-type (WT) mice, RIP3-deficient (Rip3−/−) mice, and RIP3-caspase-8 double-knockout (R3/C8−/−) mice were sensitized with OVA/alum and challenged with OVA. Fluorescence-activated cell sorting (FACS) analysis was performed for pulmonary immune cell infiltration 24 h after the last OVA challenge. (b) Representative lung hematoxylin and eosin (H&E) sections from OVA-treated WT, Rip3−/−, and Rip3−/−Casp8−/− mice. (c) Clinical scores of pulmonary disease on the basis of inflammation, eosinophils, alveolar exudates, and vascular muscle hypertrophy. (d) IgE level in the lung of OVA-treated WT, Rip3−/−, and Rip3−/−Casp8−/− mice. (e) Rip3−/− and RIP3-FADD double-knockout mice (R3/Fa−/−) were sensitized with OVA/alum and challenged with OVA. FACS analysis was performed for pulmonary immune cell infiltration 24 h after the last OVA challenge. (f) Representative lung H&E sections from OVA-treated Rip3−/− and Rip3−/−Fadd−/− mice. (g) Clinical scores of pulmonary disease on the basis of inflammation, eosinophils, alveolar exudates, and vascular muscle hypertrophy. (h) IgE level in the lung of OVA-treated Rip3−/− and Rip3−/−Fadd−/− mice. Arrow and arrowhead indicate immune cell infiltration and thick airway muscle, respectively. Each symbol indicates an individual mouse and mean±s.e.m. values are shown. Results are representative of three independent experiments for a–d and two independent experiments for e–h. *P<0.05; **P<0.01; ***P<0.001; ****P<0.0001; FADD, Fas-associated protein with death domain; NS, not significant; OVA, ovalbumin; RIP3, receptor interacting protein kinase-3.
