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. 2019 Jan 24;9:669. doi: 10.1038/s41598-018-36724-2

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Expression of DN EGFR diminishes T. gondii load in the eye and brain and enhances resistance to ocular and cerebral toxoplasmosis. Trg-Ctr and Trg-DN EGFR mice were infected with tissue cysts of the ME49 strain of T. gondii and euthanized at 14 days. (a) Retinal levels of T. gondii B1 gene were examined using qPCR. 12 mice per group pooled from 3 independent experiments. Eyes from infected Trg-Ctr showed disruption of retinal architecture, perivascular (arrow) and vitreal inflammation (arrowhead). H&E; X200. Bar, 100 μm. Histopathologic changes in the retina and brain were scored using previously described criteria (refs ^33,34). Bars are mean ± SEM of 12 mice per group from 3 pooled experiments. (b) T. gondii tissue cysts per brain. 12 mice per group pooled from 3 independent experiments. Brains from Trg-Ctr mice showed more prominent microglial nodules (arrow) and frequent tissue cysts (arrowhead). PASH original magnification x200. Bar, 100 μm. **p < 0.01, ***p < 0.001 (Student’s t test; Mann-Whitney U test).