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Updated: Mar 22, 2026

3-D Imaging and Analysis of Neurons Infected In Vivo with Toxoplasma gondii
Published on: December 9, 2014
Cerebral complement C1q activation in chronic Toxoplasma infection
Jianchun Xiao1, Ye Li1, Kristin L Gressitt1
1Stanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Blalock 1105, Baltimore, MD 21287-4933, USA.
Toxoplasma gondii infection increases brain complement factor C1q in mice. This immune response may help clear the parasite but could affect neural connectivity.
Area of Science:
- Neuroscience
- Immunology
- Parasitology
Background:
- Toxoplasma gondii (T. gondii) infection causes brain and behavioral changes.
- Complement factor C1q (C1q) is involved in immune responses and synaptic pruning in the brain.
- Both T. gondii and C1q are linked to complex brain disorders like schizophrenia.
Purpose of the Study:
- To investigate the link between T. gondii infection and C1q activation in the brain.
- To determine if T. gondii cysts trigger C1q upregulation in a rodent model.
Main Methods:
- A rodent model of chronic T. gondii infection was used.
- Cortical C1q expression was measured at RNA and protein levels.
- C1q protein localization was examined in infected brain tissue.
Main Results:
- Cortical C1q was significantly upregulated in T. gondii-infected mice compared to uninfected controls.
- C1q protein was found in the cytoplasm, near astrocytes and degenerating cysts, and along cellular processes.
- High cyst burden correlated with increased C1q expression.
Conclusions:
- Latent T. gondii infection leads to increased C1q in the brain.
- C1q activation may play a role in clearing T. gondii from the central nervous system.
- This process might impact neuronal connectivity and synaptic function.
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