Fig. 4.

Pathway for caspase-11 activation is primed upon macrophage infection by Legionella. (A) Naïve BMMs from the indicated mouse strains were infected with Legionella strains for either 2 h or 4 h. Cleaved caspase-1 in the supernatant fraction from the infected BMMs (Casp1 p10) was measured by immunoblot analysis and compared with the levels of procaspase-1 and tubulin in the BMM lysates. (B) IL-1α, IL-1β, and IL-18 levels from indicated naïve BMM culture supernatants after infection by the indicated strains of Legionella for 8 h. (C) Naïve BMM’s were derived from the mice indicated (x axis) and infected for either 2 h or 4 h with wild-type Legionella (black bars), ∆dotA (white bars), or ∆flaA (gray bars). Cell death of BMMs was determined as the percentage of LDH released compared with cells lysed with Triton X-100 (y axis). (D) BMMs derived from C57BL/6 mice, caspase-11–deficient mice (Casp1^−/−), and caspase-1/11–deficient mice (Casp1/11^−/−) mice were either left untreated (none, gray bars) or primed for 3 h by infection with a ∆dotA mutant (black bars), as indicated. Cell death of BMMs was determined as the percentage of LDH released compared with cells lysed with Triton X-100 (y axis). Data are represented as averages ± SD. *P < 0.05 compared with WT Legionella infections.