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Updated: Feb 1, 2026
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3-D Imaging and Analysis of Neurons Infected In Vivo with Toxoplasma gondii
Published on: December 9, 2014
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A Double-Edged Sword: Complement Component 3 in Toxoplasma gondii Infection
Wan-Yi Huang1,2, Ya-Pei Wang1,2, Yasser S Mahmmod3,4,5
1College of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, Guangdong, P. R. China.
Proteomics
|December 6, 2018
Summary
Toxoplasma gondii infection causes fatal central nervous system disease. In susceptible mice, complement component 3 (C3) disrupts the blood-brain barrier
Area of Science:
- Neuroscience
- Immunology
- Parasitology
Background:
- Toxoplasmosis is a fatal disease caused by *Toxoplasma gondii*.
- The mechanisms of *T. gondii*'s invasion of the central nervous system (CNS) and differential host susceptibility remain unclear.
Purpose of the Study:
- To investigate the molecular mechanisms underlying the differential susceptibility of Sprague Dawley rats and Kunming (KM) mice to *T. gondii* infection.
- To identify differentially expressed proteins (DEPs) in the brains of infected rodents.
Main Methods:
- Comparative proteomic analysis using isobaric tags for relative and absolute quantitation (iTRAQ).
- Proteomic analysis was performed on brain tissues from infected Sprague Dawley rats and KM mice, compared to healthy controls.
Main Results:
- In susceptible KM mice, *T. gondii* infection led to the upregulation of complement component 3 (C3).
- Disruption of the tight junction (TJ) pathway was observed in the brains of infected KM mice.
- Upregulated C3 is presumed to disrupt the TJ of the blood-brain barrier, facilitating *T. gondii* CNS invasion.
Conclusions:
- Complement component 3 (C3) plays a critical role in the susceptibility of KM mice to *Toxoplasma gondii* infection.
- Disruption of the blood-brain barrier's tight junctions by C3 is a key mechanism enabling *T. gondii* to invade the CNS.
- Understanding these mechanisms can inform strategies for treating toxoplasmosis.
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