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Neuroprotective Effect of Chronic Intracranial Toxoplasma gondii Infection in a Mouse Cerebral Ischemia Model
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 brai...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Society for Parasitology and Tropical Medicine
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7462801/ https://www.ncbi.nlm.nih.gov/pubmed/32871641 http://dx.doi.org/10.3347/kjp.2020.58.4.461 |
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author | Lee, Seung Hak Jung, Bong-Kwang Song, Hyemi Seo, Han Gil Chai, Jong-Yil Oh, Byung-Mo |
author_facet | Lee, Seung Hak Jung, Bong-Kwang Song, Hyemi Seo, Han Gil Chai, Jong-Yil Oh, Byung-Mo |
author_sort | Lee, Seung Hak |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-7462801 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | The Korean Society for Parasitology and Tropical Medicine |
record_format | MEDLINE/PubMed |
spelling | pubmed-74628012020-09-08 Neuroprotective Effect of Chronic Intracranial Toxoplasma gondii Infection in a Mouse Cerebral Ischemia Model Lee, Seung Hak Jung, Bong-Kwang Song, Hyemi Seo, Han Gil Chai, Jong-Yil Oh, Byung-Mo Korean J Parasitol Brief Communication 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. The Korean Society for Parasitology and Tropical Medicine 2020-08 2020-08-25 /pmc/articles/PMC7462801/ /pubmed/32871641 http://dx.doi.org/10.3347/kjp.2020.58.4.461 Text en Copyright © 2020 by The Korean Society for Parasitology and Tropical Medicine This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Brief Communication Lee, Seung Hak Jung, Bong-Kwang Song, Hyemi Seo, Han Gil Chai, Jong-Yil Oh, Byung-Mo Neuroprotective Effect of Chronic Intracranial Toxoplasma gondii Infection in a Mouse Cerebral Ischemia Model |
title | Neuroprotective Effect of Chronic Intracranial Toxoplasma gondii Infection in a Mouse Cerebral Ischemia Model |
title_full | Neuroprotective Effect of Chronic Intracranial Toxoplasma gondii Infection in a Mouse Cerebral Ischemia Model |
title_fullStr | Neuroprotective Effect of Chronic Intracranial Toxoplasma gondii Infection in a Mouse Cerebral Ischemia Model |
title_full_unstemmed | Neuroprotective Effect of Chronic Intracranial Toxoplasma gondii Infection in a Mouse Cerebral Ischemia Model |
title_short | Neuroprotective Effect of Chronic Intracranial Toxoplasma gondii Infection in a Mouse Cerebral Ischemia Model |
title_sort | neuroprotective effect of chronic intracranial toxoplasma gondii infection in a mouse cerebral ischemia model |
topic | Brief Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7462801/ https://www.ncbi.nlm.nih.gov/pubmed/32871641 http://dx.doi.org/10.3347/kjp.2020.58.4.461 |
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