Figure 1.

The role of NLRP3, ASC, and caspase-1 in inflammasome activation and cellular recruitment to the lung after influenza infection. (A–G) BM macrophages (A), BMDCs (B), or primary lung fibroblast (C) prepared from WT, NLRP3-, and caspase-1–deficient mice were infected with A/PR8 virus at MOI 2.5. Supernatant was collected 12–24 h after stimulation and analyzed for IL-1β by ELISA. WT, NLRP3-, NLRC4-, ASC-, and caspase-1–deficient mice were infected intranasally with 10³ PFU A/PR8 virus. BAL was collected by washing the trachea and lungs twice by injecting a total of 1 ml PBS containing 0.1% BSA (D and F). Lung homogenate was prepared in 2 ml PBS containing 0.1% BSA (E and G). IL-1β levels detected from the BAL or lung homogenate at different time points (D) or at 2 d p.i. (E–G) are shown. Horizontal lines show the mean. (H–I) Lung tissue was collected from the indicated groups of mice at 0 and 5 d p.i. Total lung leukocytes were enumerated. The values represent the mean of three mice per group and are expressed as the mean ± SD. Similar results were obtained from at least two separate experiments. *, P < 0.05; **, P < 0.01 versus a group of noninfected mice.