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. Author manuscript; available in PMC: 2009 Aug 1.
Published in final edited form as: Immunity. 2008 Aug;29(2):306–317. doi: 10.1016/j.immuni.2008.05.019

Figure 2. Absence of CCR2 or MCP-1 leads to increased parasite numbers, neutrophil recruitment and intestinal necrosis following T. gondii infection.

Figure 2

(A) Oral infection with T. gondii induced mild intestinal inflammation in wild type mice but extensive pathology in CCR2−/− and MCP-1−/− mice. Orally infected mice were examined at day 9 post-infection by H&E staining of paraffin sections. Normal ileum morphology was seen in noninfected C57BL/6. Infected C57BL/6 had slightly swollen villi and increased cells in the lamina propria. Lesions (asterisk) observed in the ileum of infected CCR2−/− and infected MCP-1−/− mice were characterized by disruption of the villus architecture, destruction of the inner circular layer of the tunica muscularis (ICM), and extensive replication of parasites (arrow and insets). Scale = 200 µm (15 µm in insets). Right panels are enlarged views.

(B) High numbers of neutrophils colocalized with T. gondii in the lesion areas of CCR2−/− and MCP-1−/− mice. Orally infected mice were examined at 9 days post-infection by staining with polyclonal anti-T. gondii (green) and anti-neutrophil (Ly6G, mAb 1A8) followed by Alexa-conjugated secondary antibodies. Scale bar = 20 µm.