The caspase-1 pathway controls the cell death induction of both host macrophages and intracellular parasite but not parasite proliferation.

<p>(<b>A, B, C</b>) Caspase-1 inhibitor YVAD and pan-caspase inhibitor Z-VAD (Calbiochem) were applied at respectively 50 µM and 100 µM to LEW and LEW.BNc10-F peritoneal macrophages infected 6 h with RH-YFP parasites. (<b>A</b>) Cell death was monitored by PI uptake. Histograms represent the percentage of PI positive dying cells (results indicate the difference between infected and uninfected cells). Data are means +/− SD from three independent experiments; _*: <i>p</i><0.05. (<b>B</b>) The YFP-positive infected macrophages were monitored by fluorescent microscopy. Parasite viability was evaluated through the percentage of YFP-positive infected cells 6 h post-infection. <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004005#s2" target="_blank">Results</a> were normalized according to the percentage of YFP-positive infected cells obtained in untreated LEW.BNc10-F macrophages. Columns represent mean +/− SD of three different experiments; _*: <i>p</i><0.05; _**: <i>p</i><0.01. (<b>C</b>) Intracellular growth of <i>T. gondii</i> was measured by monitoring [³H] uracil incorporation into <i>T. gondii</i>. For each treatment, results were normalized according to the values obtained in LEW.BNc10-F macrophages. Columns represent mean +/− SD of three independent experiments; _*: <i>p</i><0.05; _**: <i>p</i><0.01.