Figure 1.
NLRP3 inflammasome responses and IL‐1β production in the lung during severe IAV infection. (a–g) C57BL/6 mice were infected with 105 PFU of HKx31 as a model of severe IAV infection. (a) Percentage weight loss (mean ± s.e.m.) and survival of infected mice. (b‐g) Lungs were harvested from uninfected mice (day 0) and IAV‐infected mice on days 1 and 3 postinfection. mRNA expression of (b) Nlrp3, (c) Caspase 1, (d) Asc, (e) Il‐1β and (f) Il‐18 relative to Gapdh. Individual mice are shown as symbols and bars represent the mean. *P < 0.05, **P < 0.01; one‐way ANOVA. Data are representative of two independent experiments which were pooled (n = 8 or 9). (g) Immunoblot of NLRP3 (118‐kDa band labeled with an arrow and high‐molecular weight nonspecific band with an asterisk), procaspase‐1 (p45), caspase 1 (p20), pro‐IL‐1β (p31), IL‐1β (p17) and α‐tubulin protein. Data are representative of two independent experiments each consisting of four or five mice per group. IAV, influenza A virus; IL, interleukin; mRNA, messenger RNA; PFU, plaque‐forming units.