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. 2015 Jun 2;14(6):528–534. doi: 10.1128/EC.00276-14

FIG 5.

FIG 5

Impaired schizont-to-ring-stage transition of ptex88− parasites correlates with exacerbated splenomegaly in infected mice. (A) ptex88− parasites develop normally ex vivo, while trx2− parasites display a continuous growth delay (n.s., nonsignificant; **, P < 0.01; two-way ANOVA; n = 6). (B) Representative photographs of spleens (top, from left to right) from a naive mouse, a WT-infected mouse, a trx2−-infected mouse, and two ptex88−-infected mice (1× and 100× inoculum). Shown below is spleen weight (milligrams) according to infection. Spleens were removed 7 days after intravenous injection of 1,000 or 100,000 (100×) parasites (n.s., nonsignificant; *, P < 0.05; one-way ANOVA and Tukey's multiple-comparison test; n = 5). (C) In vivo parasite growth of WT (gray) and ptex88− (red) parasites in normal (filled squares) or splenectomized (open squares) mice (nonsignificant; two-way ANOVA; n = 3). Parasite multiplication rates were the following: WT, normal mice, 9.1; WT, splenectomized mice, 11.0; ptex88−, normal mice, 6.6; ptex88−, splenectomized mice, 6.8. (D) In vivo schizont-to-ring-stage conversion of ex vivo-cultured ptex88− parasites relative to an internal WT control after mixed inoculations of schizonts (left) or free merozoites (right). Bars, 5 μm.