Trypanosoma cruzi in the Chicken Model: Chagas-Like Heart Disease in the Absence of Parasitism

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dc.contributor.authorTeixeira, Antonio R. L.
dc.contributor.authorGomes, Clever
dc.contributor.authorNitz, Nadjar
dc.contributor.authorSousa, Alessandro O.
dc.contributor.authorAlves, Rozeneide M.
dc.contributor.authorDiniz, Maria Cambraia Guimaro
dc.contributor.authorCordeiro, Ciro
dc.contributor.authorBernal, Francisco M.
dc.contributor.authorRosa, Ana C.
dc.contributor.authorHejnar, Jiri
dc.contributor.authorLeonardecz, Eduardo
dc.contributor.authorHecht, Mariana M.
dc.date.accessioned2022-10-31T15:04:12Z
dc.date.available2022-10-31T15:04:12Z
dc.date.issued2011-03-29
dc.description.abstractBackground: The administration of anti-trypanosome nitroderivatives curtails Trypanosoma cruzi infection in Chagas disease patients, but does not prevent destructive lesions in the heart. This observation suggests that an effective treatment for the disease requires understanding its pathogenesis. Methodology/Principal Findings: To understand the origin of clinical manifestations of the heart disease we used a chicken model system in which infection can be initiated in the egg, but parasite persistence is precluded. T. cruzi inoculation into the air chamber of embryonated chicken eggs generated chicks that retained only the parasite mitochondrial kinetoplast DNA minicircle in their genome after eight days of gestation. Crossbreeding showed that minicircles were transferred vertically via the germ line to chicken progeny. Minicircle integration in coding regions was shown by targeted-primer thermal asymmetric interlaced PCR, and detected by direct genomic analysis. The kDNA-mutated chickens died with arrhythmias, shortness of breath, cyanosis and heart failure. These chickens with cardiomyopathy had rupture of the dystrophin and other genes that regulate cell growth and differentiation. Tissue pathology revealed inflammatory dilated cardiomegaly whereby immune system mononuclear cells lyse parasite-free target heart fibers. The heart cell destruction implicated a thymus-dependent, autoimmune; self-tissue rejection carried out by CD45+ , CD8cd+ , and CD8a lymphocytes. Conclusions/Significance: These results suggest that genetic alterations resulting from kDNA integration in the host genome lead to autoimmune-mediated destruction of heart tissue in the absence of T. cruzi parasites.en_US
dc.description.sponsorshipThe authors thank Nancy R Sturm for helpful discussions and comments on the manuscript. We are indebted to Prof. Dusand Kordis for donation of the XeCrs primer sets used.en_US
dc.description.urihttps://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0001000en_US
dc.format.extent18 pagesen_US
dc.genrejournal articlesen_US
dc.identifierdoi:10.13016/m2lthe-1d3g
dc.identifier.citationTeixeira ARL, Gomes C, Nitz N, Sousa AO, Alves RM, Guimaro MC, et al. (2011) Trypanosoma cruzi in the Chicken Model: Chagas-Like Heart Disease in the Absence of Parasitism. PLoS Negl Trop Dis 5(3): e1000. https://doi.org/10.1371/journal.pntd.0001000en_US
dc.identifier.urihttps://doi.org/10.1371/journal.pntd.0001000
dc.identifier.urihttp://hdl.handle.net/11603/26245
dc.language.isoen_USen_US
dc.publisherPLOSen_US
dc.relation.isAvailableAtThe University of Maryland, Baltimore County (UMBC)
dc.relation.ispartofUMBC Office of the Dean of the College of Natural and Mathematical Sciences
dc.rightsThis item is likely protected under Title 17 of the U.S. Copyright Law. Unless on a Creative Commons license, for uses protected by Copyright Law, contact the copyright holder or the author.en_US
dc.rightsAttribution 4.0 International (CC BY 4.0)*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.titleTrypanosoma cruzi in the Chicken Model: Chagas-Like Heart Disease in the Absence of Parasitismen_US
dc.typeTexten_US
dcterms.creatorhttps://orcid.org/0000-0002-2633-9710en_US

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