A double‐edged sword: Complement component 3 in toxoplasma gondii infection
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
Fecha de publicación
2018-12-04ISSN
1615-9853
Resumen
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.
Tipo de documento
Artículo
Versión del documento
Versión aceptada
Lengua
English
Páginas
34
Publicado por
Wiley
Publicado en
Proteomics
Citación
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
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