Korean J Parasitol.  2020 Aug;58(4):461-466. 10.3347/kjp.2020.58.4.461.

Neuroprotective Effect of Chronic Intracranial Toxoplasma gondii Infection in a Mouse Cerebral Ischemia Model

  • 1Department of Rehabilitation Medicine, Asan Medical Center, College of Medicine, University of Ulsan, Seoul 05505, Korea
  • 2Institute of Parasitic Diseases, Korea Association of Health Promotion, Seoul 07653, Korea
  • 3Department of Rehabilitation Medicine, Seoul National University Hospital, 03080 Seoul, Korea
  • 4Department of Tropical Medicine and Parasitology, Seoul National University College of Medicine, Seoul 03080, Korea


Toxoplasma gondii is an obligate intracellular protozoan parasite that can invade various organs in the host body, including the central nervous system. Chronic intracranial T. gondii is known to be associated with neuroprotection against neurodegenerative diseases through interaction with host brain cells in various ways. The present study investigated the neuroprotective effects of chronic T. gondii infection in mice with cerebral ischemia experimentally produced by middle cerebral artery occlusion (MCAO) surgery. The neurobehavioral effects of cerebral ischemia were assessed by measurement of Garcia score and Rotarod behavior tests. The volume of brain ischemia was measured by triphenyltetrazolium chloride staining. The expression levels of related genes and proteins were determined. After cerebral ischemia, corrected infarction volume was significantly reduced in T. gondii infected mice, and their neurobehavioral function was significantly better than that of the uninfection control group. Chronic T. gondii infection induced the expression of hypoxia-inducible factor 1-alpha (HIF-1α) in the brain before MCAO. T. gondii infection also increased the expression of vascular endothelial growth factor after the cerebral ischemia. It is suggested that chronic intracerebral infection of T. gondii may be a potential preconditioning strategy to reduce neural deficits associated with cerebral ischemia and induce brain ischemic tolerance through the regulation of HIF-1α expression.


cerebral ischemia; ischemic tolerance; neuroprotection
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