| Literature DB >> 30515942 |
Wan-Yi Huang1,2, Ya-Pei Wang1,2, Yasser S Mahmmod3,4,5, Jun-Jie Wang1,2, Tang-Hui Liu1,2, Yu-Xiang Zheng1,2, Xue Zhou1,2, Xiu-Xiang Zhang6, Zi-Guo Yuan1,2,7.
Abstract
Sprague Dawley rats and Kunming (KM) mice are artificially infected with type II Toxoplasma gondii strain Prugniaud (Pru) to generate toxoplasmosis, which is a fatal disease mediated by T. gondii invasion of the central nervous system (CNS) by unknown mechanisms. The aim is to explore the mechanism of differential susceptibility of mice and rats to T. gondii infection. Therefore, a strategy of isobaric tags for relative and absolute quantitation (iTRAQ) is established to identify differentially expressed proteins (DEPs) in the rats' and the mice's brains compared to the healthy groups. In KM mice, which is susceptible to T. gondii infection, complement component 3 (C3) is upregulated and the tight junction (TJ) pathway shows a disorder. It is presumed that T. gondii-stimulated C3 disrupts the TJ of the blood-brain barrier in the CNS. This effect allows more T. gondii passing to the brain through the intercellular space.Entities:
Keywords: Toxoplasma gondii; blood-brain barrier; central nervous system; complement component 3; paracellular entry mechanism
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Year: 2019 PMID： 30515942 DOI： 10.1002/pmic.201800271
Source DB: PubMed Journal: Proteomics ISSN： 1615-9853 Impact factor: 3.984