Role of dystrophin in acute Trypanosoma cruzi infection
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2014
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Previous studies have demonstrated loss/reduction of dystrophin in cardiomyocytes in both acute and chronic stages of experimental Try panosoma cruzi (T. cruzi) infection in mice. The mechanisms responsible for dystrophin disruption in the hearts of mice acutely infected with T.
cruzi are not completely understood. The present in vivo and in vitro studies were undertaken to evaluate the role of inflammation in dystrophin
disruption and its correlation with the high mortality rate during acute infection. C57BL/6 mice were infected with T. cruzi and killed 14, 20 and
26 days post infection (dpi). The intensity of inflammation, cardiac expression of dystrophin, calpain-1, NF-kB, TNF-a, and sarcolemmal
permeability were evaluated. Cultured neonatal murine cardiomyocytes were incubated with serum, collected at the peak of cytokine production
and free of parasites, from T. cruzi-infected mice and dystrophin, calpain-1, and NF-kB expression analyzed. Dystrophin disruption occurs at the
peak of mortality and inflammation and is associated with increased expression of calpain-1, TNF-a, NF-kB, and increased sarcolemmal
permeability in the heart of T. cruzi-infected mice at 20 dpi confirmed by in vitro studies. The peak of mortality occurred only when significant
loss of dystrophin in the hearts of infected animals occurred, highlighting the correlation between inflammation, dystrophin loss and mortality.
© 2014 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
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Trypanosoma cruzi, Chagas disease, Dystrophin, Inflammation, Cardiomyocytes;, Calpain-1
Citação
MALVESTIO, Lygia M. et al. Role of dystrophin in acute Trypanosoma cruzi infection. Microbes and Infection, Paris, v. 16, n. 9, p. 97-105, 2014. DOI: 10.1016/j.micinf.2014.07.010. Disponível em: https://www.sciencedirect.com/science/article/pii/S1286457914000975. Acesso em: 6 fev. 2025.