Expression and production of cardiac angiogenic mediators depend on the Trypanosoma cruzi-genetic population in experimental C57BL/6 mice infection.
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2017
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Abstract
Mammalian cardiac cells are important targets to the protozoan Trypanosoma cruzi. The inflammatory reaction in
the host aims at eliminating this parasite, can lead to cell destruction, fibrosis and hypoxia. Local hypoxia iswelldefined
stimulus to the production of angiogenesis mediators. Assuming that different genetic T. cruzi populations
induce distinct inflammation and disease patterns, the current study aims to investigate whether the production
of inflammatory and angiogenic mediators is a parasite strain-dependent condition. C57BL/6 mice were
infectedwith the Y and Colombian strains of T. cruzi and euthanized at the 12th and 32nd days, respectively. The
blood and heart tissue were processed in immune assays and/or qPCR (TNF, IL-17, IL-10, CCL2, CCL3, CCL5, CCR2,
CCR5 and angiogenic factors VEGF, Ang-1, Ang-2) and in histological assays. The T. cruzi increased the inflammatory
and angiogenicmediators in the infectedmicewhen theywere compared to non-infected animals.However,
the Colombian strain has led to higher (i) leukocyte infiltration, (ii) cardiac TNF and CCL5 production/expression,
(iii) cardiac tissue parasitism, and to higher (iv) ratio between heart/body weights. On the other hand, the Colombian
strain has caused lower production and expression VEGF, Ang-1 and Ang-2, when it was compared to
the Y strain of the parasite. The present study highlights that the T. cruzi-genetic population defines the pattern
of angiogenic/inflammatory mediators in the heart tissue, and that itmay contribute to themagnitude of the cardiac
pathogenesis. Besides, such assumption opens windows to the understanding of the angiogenic mediator's
role in association with the experimental T. cruzi infection.
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Inflammation
Citation
BAJRACHARYA, D. S. et al. Expression and production of cardiac angiogenic mediators depend on the Trypanosoma cruzi-genetic population in experimental C57BL/6 mice infection. Microvascular Research, v. 110, p. 56-63, 2017. Disponível em: <http://www.sciencedirect.com/science/article/pii/S002628621630139X>. Acesso em: 15 set. 2017.