FIGURE 7.

Inflammasome-independent role for NLRP3 during innate antihelminth responses in the lung. WT and Nlrp3^−/− mice were infected with N. brasiliensis (Nb), and on day 2 postinfection (A), intracellular pro–IL-1β levels were measured in alveolar (Alv.) Mφs by flow cytometry, (B) released IL-1β in the BALF was quantified by ELISA, and (C) frequency of active caspase-1 was measured ex vivo in BAL alveolar Mφs, neutrophils, and eosinophils by FAM-FLICA fluorescence. (D) Day 2 postinfection L4 lung-stage larvae and day 6 adult intestinal worms were counted in WT, Casp1/11^−/−, and Nlrp3^−/− mice. (E) WT mice were treated with the caspase-1 inhibitor VX-765, and lung (day 2) and intestinal (day 4) worm burdens were measured. WT mice were treated with the NLRP3 inhibitor MCC950 during N. brasiliensis infection, and (F) BAL neutrophils and eosinophils were quantified and (G) Chil3 (Ym1) expression in the lung was measured by qRT-PCR. (H) Lung larval burdens (day 2) and intestinal (day 6) worm burdens were counted following MCC950 treatment and N. brasiliensis infection. Data are representative (A–C and H; mean ± SEM) or pooled (D–G; mean ± SEM) from two or three individual experiments with three to six mice per group (per experiment). *p < 0.05, **p < 0.01, ****p < 0.0001, one-way ANOVA and Tukey–Kramer post hoc test.