A double‐edged sword: Complement component 3 in toxoplasma gondii infection
Author
Huang, Wan‐Yi
Wang, Ya‐Pei
Mahmmod, Yasser S.
Wang, Jun‐Jie
Liu, Tang‐Hui
Zheng, Yu‐Xiang
Zhou, Xue
Zhang, Xiu‐Xiang
Yuan, Zi‐Guo
Publication date
2018-12-04ISSN
1615-9853
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.
Document Type
Article
Document version
Accepted version
Language
English
Pages
34
Publisher
Wiley
Is part of
Proteomics
Citation
Huang, Wan‐Yi, Ya‐Pei Wang, Yasser S. Mahmmod, Jun‐Jie Wang, Tang‐Hui Liu, Yu‐Xiang Zheng, Xue Zhou, Xiu‐Xiang Zhang, and Zi‐Guo Yuan. 2019. "A Double‐Edged Sword: Complement Component 3 In Toxoplasma Gondii Infection". PROTEOMICS 19 (3): 1800271. Wiley. doi:10.1002/pmic.201800271.
Program
Sanitat Animal
This item appears in the following Collection(s)
- ARTICLES CIENTÍFICS [2831]
Except where otherwise noted, this item's license is described as http://creativecommons.org/licenses/by-nc-nd/4.0/