Abstract

The objective of this study was to evaluate the histopathological changes caused by infection with the Colombian strain of Trypanosoma cruzi (T. cruzi) in the acute and chronic experimental phases. C57Bl/6 mice were infected with 1000 trypomastigote forms of the Colombian strain of T. cruzi. After 30 days (acute phase) and 90 days (early chronic phase) of infection, the animals were euthanized, and the colon was collected and divided into two parts: proximal and distal. The distal portion was used for histopathological analysis, whereas the proximal portion was used for quantification of pro- and anti-inflammatory cytokines. In addition, the weight of the animals and parasitemia were assessed. The infection induced gradual weight loss in the animals. In addition, the infection induced an increase in interferon gamma (IFNγ) and tumor necrosis factor-alpha (TNF-α) in the intestine in the acute phase, in which this increase continued until the early chronic phase. The same was observed in relation to the presence of intestinal inflammatory infiltrates. In relation to interleukin (IL)-10, there was an increase only in the early chronic phase. The Colombian strain infection was also able to induce neuronal loss in the myenteric plexus and deposition of the collagen fibers during the acute phase. The Colombian strain of T. cruzi is capable of causing histopathological changes in the intestine of infected mice, especially in inducing neuronal destructions. Thus, this strain can also be used to study the intestinal form of Chagas disease in experimental models.

Highlights

  • More than 100 years after the discovery of the etiologic agent of Chagas disease (CD), Trypanosoma cruzi, the disease still has a great socioeconomic impact

  • The focus of this study was to evaluate whether the Colombian strain was capable of inducing immunopathological changes in the intestines of C57Bl/6 mice during the acute and early chronic experimental phases

  • Our results show that during the acute stage, there are intestinal changes, such as increased inflammatory infiltrate, neuronal destruction, and collagen deposition, along with the maintenance of the inflammatory process with proinflammatory cytokines until the early chronic phase

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Summary

Introduction

More than 100 years after the discovery of the etiologic agent of Chagas disease (CD), Trypanosoma cruzi, the disease still has a great socioeconomic impact This disease is estimated to cost approximately $627 million per year for global public health [1]. Mice of the C57BL/6 strain infected with the Y strain, for example, show changes in the width of the colon and thickness of the muscle layer and an increase in the inflammatory infiltrate in the intestine, as well as tissue parasitism, myositis, ganglionitis, and periganglionitis during the acute experimental phase [9]. Infection by this strain leads to neuronal decrease in experimental models in both the acute and chronic phases [5, 12], which is a milestone in the progression of the megacolon in humans [13, 14]

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