Cell death pattern in cerebellum neurons infected with Toxoplasma gondii

Samar el-Sagaff1, Hala Said Salem, Wafa Nichols

  • 1Department of Anatomy, Faculty of Medicine, King Abdel Aziz University, Jeddah, Saudi Arabia.

Insights

Toxoplasma gondii infection causes neuro-pathological changes in the mouse cerebellum, including necrosis and Purkinje cell loss. Apoptosis may occur due to factors other than the Bax marker in toxoplasmosis.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Toxoplasma gondii infection is a growing concern, necessitating research into its role in cell death for disease prevention.
  • Acquired toxoplasmosis can lead to neuro-pathological alterations, particularly within the cerebellum cortex.

Purpose of the Study:

  • To investigate the neuro-pathological changes in the cerebellum cortex of mice infected with Toxoplasma gondii.
  • To examine the expression of the pro-apoptotic marker Bax and its correlation with observed cell death.

Main Methods:

  • Adult Balb C mice were infected with the T. gondii RH strain via intraperitoneal injection.
  • Immuno-histochemical staining for Bax and Hematoxylin and Eosin staining were used to analyze cerebellum cortex layers.
  • Morphometric analysis was performed to quantify changes in cell viability and layer proportions.

Main Results:

  • Focal necrosis and vasculitis were observed in the cerebellum, attributed to hypoxic ischemia.
  • Purkinje cells showed significant disfigurement, focal loss, and apoptotic/necrotic changes.
  • While Purkinje cells were most affected, morphometric analysis showed no significant difference in viable to non-viable cell ratios between groups. A significant change in the molecular layer to internal granular layer depth proportion was noted (p=0.05).
  • Bax expression did not consistently correlate with Hematoxylin and Eosin staining results.

Conclusions:

  • Toxoplasmosis appears to resist apoptosis, suggesting the parasite benefits from this mechanism.
  • The observed apoptosis following infection might be mediated by proteins other than Bax.

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