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. 2013 Oct 10;9(10):e1003706. doi: 10.1371/journal.ppat.1003706

Figure 2. Cxcr3−/− mice are susceptible to severe intestinal pathology following oral T. gondii infection.

Figure 2

WT and CXCR3-deficient mice were orally inoculated with 30 ME49 cysts (A) or 50 cysts (B) of T. gondii and monitored for survival. In another set of experiments (C–J), mice were orally inoculated with 30 ME49 cysts, and tissues were collected at Day 10 post-infection. (C) Gross intestinal lesions in representative WT and CXCR3 KO mice. (D) Average lengths of noninfected (NI) and infected (INF) WT and Cxcr3 −/− small intestines (NI WT, n = 5; NI KO, n = 3; INF WT, n = 8, INF KO: n = 7). E–H, H&E stained sections of small intestines from infected WT (E and G) and KO (F and H) mice. In panel G, the arrow points to an area of inflammatory cell influx. In panel H, the yellow arrow indicates an area of vascular congestion, and the red arrow indicates a necrotic villus. Blind scoring was performed on H&E stained intestine sections for inflammation (I) and damage (J) criteria (WT: n = 14; KO: n = 13; * p<0.05, ** p<0.01, *** p<0.001). Pooled data are represented as mean +/− SEM.