A double‐edged sword: Complement component 3 in toxoplasma gondii infection
Visualitza/Obre
Autor/a
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
Data de publicació
2018-12-04ISSN
1615-9853
Resum
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.
Tipus de document
Article
Versió del document
Versió acceptada
Llengua
English
Pàgines
34
Publicat per
Wiley
Publicat a
Proteomics
Citació
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.
Programa
Sanitat Animal
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