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A Double‐Edged Sword: Complement Component 3 in Toxoplasma gondii Infection
Author(s) -
Huang WanYi,
Wang YaPei,
Mahmmod Yasser S.,
Wang JunJie,
Liu TangHui,
Zheng YuXiang,
Zhou Xue,
Zhang XiuXiang,
Yuan ZiGuo
Publication year - 2019
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.201800271
Subject(s) - toxoplasma gondii , toxoplasmosis , biology , immunology , central nervous system , complement (music) , blood–brain barrier , virology , neuroscience , antibody , phenotype , genetics , gene , complementation
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.