The neurotropic schistosome vs experimental autoimmune encephalomyelitis: are there any winners?

The incidences of multiple sclerosis have risen worldwide, yet neither the trigger nor efficient treatment is known. Some research is dedicated to looking for treatment by parasites, mainly by helminths. However, little is known about the effect of helminths that infect the nervous system. Therefore...

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Main Authors: Barbora Šmídová, Martin Majer, Jan Novák, Alena Revalová, Petr Horák, Tomáš Macháček
Format: Article
Language:English
Published: Cambridge University Press 2024-04-01
Series:Parasitology
Subjects:
Online Access:https://www.cambridge.org/core/product/identifier/S0031182024000210/type/journal_article
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author Barbora Šmídová
Martin Majer
Jan Novák
Alena Revalová
Petr Horák
Tomáš Macháček
author_facet Barbora Šmídová
Martin Majer
Jan Novák
Alena Revalová
Petr Horák
Tomáš Macháček
author_sort Barbora Šmídová
collection DOAJ
description The incidences of multiple sclerosis have risen worldwide, yet neither the trigger nor efficient treatment is known. Some research is dedicated to looking for treatment by parasites, mainly by helminths. However, little is known about the effect of helminths that infect the nervous system. Therefore, we chose the neurotropic avian schistosome Trichobilharzia regenti, which strongly promotes M2 polarization and tissue repair in the central nervous system, and we tested its effect on the course of experimental autoimmune encephalomyelitis (EAE) in mice. Surprisingly, the symptoms of EAE tended to worsen after the infection with T. regenti. The infection did not stimulate tissue repair, as indicated by the similar level of demyelination. Eosinophils heavily infiltrated the infected tissue, and the microglia number increased as well. Furthermore, splenocytes from T. regenti-infected EAE mice produced more interferon (IFN)-γ than splenocytes from EAE mice after stimulation with myelin oligodendrocyte glycoprotein. Our research indicates that the combination of increased eosinophil numbers and production of IFN-γ tends to worsen the EAE symptoms. Moreover, the data highlight the importance of considering the direct effect of the parasite on the tissue, as the migrating parasite may further tissue damage and make tissue repair even more difficult.
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spelling doaj.art-1831fd3501da48a58fc23723ddfcf3af2024-04-22T03:08:08ZengCambridge University PressParasitology0031-18201469-81612024-04-0115141242010.1017/S0031182024000210The neurotropic schistosome vs experimental autoimmune encephalomyelitis: are there any winners?Barbora Šmídová0https://orcid.org/0000-0002-5746-9657Martin Majer1https://orcid.org/0000-0001-7570-0771Jan Novák2https://orcid.org/0000-0001-8645-9389Alena Revalová3Petr Horák4https://orcid.org/0000-0001-9820-5044Tomáš Macháček5https://orcid.org/0000-0002-6310-4099Department of Parasitology, Faculty of Science, Charles University, Prague, CzechiaDepartment of Parasitology, Faculty of Science, Charles University, Prague, CzechiaInstitute of Immunology and Microbiology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, CzechiaDepartment of Parasitology, Faculty of Science, Charles University, Prague, CzechiaDepartment of Parasitology, Faculty of Science, Charles University, Prague, CzechiaDepartment of Parasitology, Faculty of Science, Charles University, Prague, CzechiaThe incidences of multiple sclerosis have risen worldwide, yet neither the trigger nor efficient treatment is known. Some research is dedicated to looking for treatment by parasites, mainly by helminths. However, little is known about the effect of helminths that infect the nervous system. Therefore, we chose the neurotropic avian schistosome Trichobilharzia regenti, which strongly promotes M2 polarization and tissue repair in the central nervous system, and we tested its effect on the course of experimental autoimmune encephalomyelitis (EAE) in mice. Surprisingly, the symptoms of EAE tended to worsen after the infection with T. regenti. The infection did not stimulate tissue repair, as indicated by the similar level of demyelination. Eosinophils heavily infiltrated the infected tissue, and the microglia number increased as well. Furthermore, splenocytes from T. regenti-infected EAE mice produced more interferon (IFN)-γ than splenocytes from EAE mice after stimulation with myelin oligodendrocyte glycoprotein. Our research indicates that the combination of increased eosinophil numbers and production of IFN-γ tends to worsen the EAE symptoms. Moreover, the data highlight the importance of considering the direct effect of the parasite on the tissue, as the migrating parasite may further tissue damage and make tissue repair even more difficult.https://www.cambridge.org/core/product/identifier/S0031182024000210/type/journal_articledemyelinationEAEeosinophiliaexperimental autoimmune encephalomyelitisIFN-γneurotropic parasiteneurotropic schistosomeTrichobilharzia regenti
spellingShingle Barbora Šmídová
Martin Majer
Jan Novák
Alena Revalová
Petr Horák
Tomáš Macháček
The neurotropic schistosome vs experimental autoimmune encephalomyelitis: are there any winners?
Parasitology
demyelination
EAE
eosinophilia
experimental autoimmune encephalomyelitis
IFN-γ
neurotropic parasite
neurotropic schistosome
Trichobilharzia regenti
title The neurotropic schistosome vs experimental autoimmune encephalomyelitis: are there any winners?
title_full The neurotropic schistosome vs experimental autoimmune encephalomyelitis: are there any winners?
title_fullStr The neurotropic schistosome vs experimental autoimmune encephalomyelitis: are there any winners?
title_full_unstemmed The neurotropic schistosome vs experimental autoimmune encephalomyelitis: are there any winners?
title_short The neurotropic schistosome vs experimental autoimmune encephalomyelitis: are there any winners?
title_sort neurotropic schistosome vs experimental autoimmune encephalomyelitis are there any winners
topic demyelination
EAE
eosinophilia
experimental autoimmune encephalomyelitis
IFN-γ
neurotropic parasite
neurotropic schistosome
Trichobilharzia regenti
url https://www.cambridge.org/core/product/identifier/S0031182024000210/type/journal_article
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