Trypanosoma cruzi in the chicken model: Chagas-like heart disease in the absence of parasitism

0365173 - ÚMG 2012 RIV US eng J - Článek v odborném periodiku
Teixeira, A.R.L. - Gomes, C. - Nitz, N. - Sousa, A.O. - Alvez, R.M. - Guimaro, M.C. - Cordeiro, C. - Bernal, F.M. - Rosa, A.C. - Hejnar, Jiří - Leonardecz, E. - Hecht, M.M.
Trypanosoma cruzi in the chicken model: Chagas-like heart disease in the absence of parasitism.
PLoS Neglected Tropical Diseases. Roč. 5, č. 3 (2011), e1000. ISSN 1935-2735. E-ISSN 1935-2735
Výzkumný záměr: CEZ:AV0Z50520514
Klíčová slova: Chagas disease * Trypanosoma cruzi * kDNA minicircles * inbred chicken
Kód oboru RIV: EB - Genetika a molekulární biologie
Impakt faktor: 4.716, rok: 2011

Destructive lesions in the heart are a substantial part of Chagas disease pathogenesis. To understand the origin of the heart disease we used a chicken model system in which infection with the pathogen, Trypanosoma cruzi, can be initiated in the egg, but parasite persistence is precluded. In ovo infection generated parasite-free chicks that retained only the mitochondrial kinetoplast DNA minicircle (kDNA) in their genome. Crossbreeding showed that kDNA was transferred vertically to chicken progeny. kDNA integration in coding regions of dystrophin and other genes was shown by cloning the insert together with adjacent chicken sequences. The pathology of kDNA-mutated chickens included heart failure, inflammatory cardiomegaly, and immune attack of heart fibres carried out by CD45(+), CD8γδ(+), and CD8α lymphocytes. We suggest that genetic alterations resulting from kDNA integration lead to autoimmune-mediated destruction of heart tissue in the absence of T. cruzi parasites.
Trvalý link: http://hdl.handle.net/11104/0200477