Neuronal Parasitism, Early Myenteric Neurons Depopulation and Continuous Axonal Networking Damage as Underlying Mechanisms of the Experimental Intestinal Chagas' Disease.

Autor:	Ricci MF; Departament of Pathology, Federal University of Minas Gerais, Belo Horizonte, Brazil., Béla SR; Departament of Pathology, Federal University of Minas Gerais, Belo Horizonte, Brazil.; Departament of Biological and Exact Sciences, Federal University of Ouro Preto, Ouro Preto, Brazil., Moraes MM; Departament of Pathology, Federal University of Minas Gerais, Belo Horizonte, Brazil., Bahia MT; Departament of Biological and Exact Sciences, Federal University of Ouro Preto, Ouro Preto, Brazil., Mazzeti AL; Departament of Biological and Exact Sciences, Federal University of Ouro Preto, Ouro Preto, Brazil., Oliveira ACS; Department of Morphology, Federal University of Minas Gerais, Belo Horizonte, Brazil., Andrade LO; Department of Morphology, Federal University of Minas Gerais, Belo Horizonte, Brazil., Radí R; Departament of Bioquímica, Facultad de Medicina, Center for Free Radical and Biomedical Research, Universidad de La Republica Montevideo, Montevideo, Uruguay., Piacenza L; Departament of Bioquímica, Facultad de Medicina, Center for Free Radical and Biomedical Research, Universidad de La Republica Montevideo, Montevideo, Uruguay., Arantes RME; Departament of Pathology, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Jazyk:	angličtina
Zdroj:	Frontiers in cellular and infection microbiology [Front Cell Infect Microbiol] 2020 Oct 15; Vol. 10, pp. 583899. Date of Electronic Publication: 2020 Oct 15 (Print Publication: 2020).
DOI:	10.3389/fcimb.2020.583899
Abstrakt:	There 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. (Copyright © 2020 Ricci, Béla, Moraes, Bahia, Mazzeti, Oliveira, Andrade, Radí, Piacenza and Arantes.)
Databáze:	MEDLINE
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