FIGURE 2.
IL-1β secretion induced by C. albicans is dependent on the Nlrp3 inflammasome. A, LPS-primed BMM from WT, Nlrp3-, ASC-, caspase-1-, or Nlrc4-deficient mice were stimulated for 6 h with or without C. albicans strain FC20 at an MOI of 1:10. Culture supernatants were collected and IL-1β secretion quantified by ELISA. Determinations were performed in triplicate and expressed as the mean ± SEM. Results are representative of two separate experiments. B, Lysates from LPS- primed Mϕ from WT, Nlrp3-, ASC-, caspase-1-, or Nlrc4-deficient mice were collected after 6h exposure to C. albicans strain FC20 and immunoblotted with antibodies against the p10 subunit of caspase-1, IL-1β and GAPDH. Results are representative of two separate experiments. C, WT (n=4) and Nlrp3−/− (n=4) mice were infected i.v. with 5 × 105 CFU of C. albicans strain FC20. After 6 days C. albicans colonization was assessed in the left kidney, spleen and liver. Data are expressed as the mean ± SEM.