Neuronal parasitism, early myenteric neurons depopulation and continuous axonal networking damage as underlying mechanisms of the experimental intestinal Chagas' disease.

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dc.contributor.authorRicci, Mayra Fernanda
dc.contributor.authorBéla, Samantha Ribeiro
dc.contributor.authorMoraes, Michele Macedo
dc.contributor.authorBahia, Maria Terezinha
dc.contributor.authorMazzeti, Ana Lia
dc.contributor.authorOliveira, Anny Carolline Silva
dc.contributor.authorOliveira, Luciana Souza de
dc.contributor.authorRadi, Rafael
dc.contributor.authorPiacenza, Lucía
dc.contributor.authorArantes, Rosa Maria Esteves
dc.date.accessioned2021-11-22T14:06:25Z
dc.date.available2021-11-22T14:06:25Z
dc.date.issued2020pt_BR
dc.description.abstractThere is a growing consensus that the balance between the persistence of infection and the host immune response is crucial for chronification of Chagas heart disease. Extrapolation for chagasic megacolon is hampered because research in humans and animal models that reproduce intestinal pathology is lacking. The parasite-host relationship and its consequence to the disease are not well-known. Our model describes the temporal changes in the mice intestine wall throughout the infection, parasitism, and the development of megacolon. It also presents the consequence of the infection of primary myenteric neurons in culture with Trypanosoma cruzi (T. cruzi). Oxidative neuronal damage, involving reactive nitrogen species induced by parasite infection and cytokine production, results in the denervation of the myenteric ganglia in the acute phase. The long-term inflammation induced by the parasite’s DNA causes intramuscular axonal damage, smooth muscle hypertrophy, and inconsistent innervation, affecting contractility. Acute phase neuronal loss may be irreversible. However, the dynamics of the damages revealed herein indicate that neuroprotection interventions in acute and chronic phases may help to eradicate the parasite and control the inflammatory-induced increase of the intestinal wall thickness and axonal loss. Our model is a powerful approach to integrate the acute and chronic events triggered by T. cruzi, leading to megacolon.pt_BR
dc.identifier.citationRICCI, M. F. et al. Neuronal parasitism, early myenteric neurons depopulation and continuous axonal networking damage as underlying mechanisms of the experimental intestinal Chagas' disease. Frontiers in Cellular and Infection Microbiology, v. 10, p. 1-25, out. 2020. Disponível em: <https://www.frontiersin.org/articles/10.3389/fcimb.2020.583899/full>. Acesso em: 10 jun. 2021.pt_BR
dc.identifier.doihttps://doi.org/10.3389/fcimb.2020.583899pt_BR
dc.identifier.issn2235-2988
dc.identifier.urihttp://www.repositorio.ufop.br/jspui/handle/123456789/13997
dc.language.isoen_USpt_BR
dc.rightsabertopt_BR
dc.rights.licenseThis is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. Source: The article PDF.pt_BR
dc.subjectTrypanosoma cruzipt_BR
dc.subjectPathogenesispt_BR
dc.subjectExperimental modelpt_BR
dc.subjectNitric oxide (NO)pt_BR
dc.subjectEnteric nervous system (ENS)pt_BR
dc.titleNeuronal parasitism, early myenteric neurons depopulation and continuous axonal networking damage as underlying mechanisms of the experimental intestinal Chagas' disease.pt_BR
dc.typeArtigo publicado em periodicopt_BR
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