Figure 3.

P2X7 receptor activation triggers T. gondii elimination via a canonical (but not via a non-canonical) inflammasome. Bone marrow-derived macrophages (BMDMs) from C57BL/6 (wild-type), and from Caspase-11^−/− and Caspase1/11^−/−knockout mice (lacking non-canonical and canonical inflammasome effectors, respectively) were infected with T. gondii tachyzoites for 2 h and then kept untreated, or were treated 3 mM extracellular ATP for 30 min. Then, cells were incubated at 37°C for a total of 18 h, and stained with Panoptic, for light microscopy observation [(A); representative images of three independent experiments] and for the quantification of the % of infection (B) and the infection index (C). We observed reduced parasite load in wild-type and Caspase-11^−/− BMDMs, but not in Caspase-1/11^−/− cells. Black arrows indicate parasitophorous vacuoles containing T. gondii tachyzoites. Micrographs are representative of three independent experiments. Data represent mean ± SEM of three independent experiments performed in triplicates. ***p ≤ 0.001 vs. untreated (by two-tailed t-test).