Fig. 6: Deficient inflammasome activation in RV-C15-infected immature mice. | Mucosal Immunology

Fig. 6: Deficient inflammasome activation in RV-C15-infected immature mice.

From: Deficient inflammasome activation permits an exaggerated asthma phenotype in rhinovirus C-infected immature mice

Fig. 6

Six-day-old C57BL/6 mice were inoculated with sham, RV-A1B, or RV-C15. a One day after infection, whole lungs were homogenized within the lysis buffer and subjected to western blot. Anti-mouse-IL-1β recognizes pro-IL-1β and its bioactive form IL-1β. Anti-mouse-caspase-1 detects both caspase-1 and its cleaved form, caspase-1 p12. b Group mean relative expression levels were normalized to β-actin. (N = 3 from three experiments, mean ± SEM, *different from sham, †different from RV-A1B, p < 0.05, one-way ANOVA.) c mRNA expression was measured 1 day later. (N = 6 from two experiments, mean ± SEM, *different from sham, p < 0.05, one-way ANOVA with Tukey’s multiple comparisons test.) d Lung pro-IL-1β+ cells in RV-infected 6-day-old mice. Pro-IL-1β+ cells were identified 1 day after infection. Pro-IL-1β+/CD45+, pro-IL-1β+/F4/80+, and pro-IL-1β+/active caspase-1+ cells were analyzed as a percentage of live cells, respectively (n = 4, mean ± SEM, *different from sham, †different from RV-A1B, p < 0.05, one-way ANOVA).

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