Avaliação da produção de BMP2 no intestino de camundongos infectados com Trypanosoma cruzi

• Autor(a) principal: Carmo Neto, José Rodrigues do
• Data de Publicação: 2020
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório Institucional da UFG
• Texto Completo: http://repositorio.bc.ufg.br/tede/handle/tede/11288
• topic: Doença de Chagas; BMP2; Intestino; Sistema nervoso entérico; Enteric nervous system; Chagas disease; BMP2; Intestine; CIENCIAS BIOLOGICAS::PARASITOLOGIA::ENTOMOLOGIA E MALACOLOGIA DE PARASITOS E VETORES

One of the main late complications of Chagas' disease (CD) is the megacolon, affecting approximately 10% of symptomatic patients. However, studies are needed to understand mechanisms involved in the progression of this condition in the chronic phase of CD. Myenteric plexus neurons are known to be essential for the control of intestinal motility. Through infection by Trypanosoma cruzi (T. cruzi), the inflammatory profile that sets in is involved in neural destruction. One of the proteins related to the maintenance of nerve cells in the myenteric plexus is the type 2 morphogenetic protein (BMP2), produced mainly by muscle macrophages. The homeostasis of the BMP2/macrophage ratio is directly involved with intestinal motility and the maintenance of organ function. Thus, the aim of this study was to correlate the production of intestinal BMP2 with the production of cytokines and histopathological changes in C57Bl / 6 mice. infected by the T. cruzi Y strain in the periods of 30 and 90 days of infection. The mice were infected with 1000 blood trypomastigote forms. After the infection period, the mice were euthanized and the spleen and intestine were collected. The intestine was divided in two, one fragment was used for histological analysis and the other for quantification of TNF-α, IFN-γ, IL-10 and BMP2, as well as the spleen. Infection with strain Y induced an increase in the production of TNF-α, IFN-γ and BMP2 in the intestine after 30 days of infection, as well as an increase in the inflammatory infiltrate and a decrease in the number of neurons in the myenteric plexus. Collagen deposition increased gradually throughout the infection, demonstrated at 90 days of infection. It was observed that the increase in BMP2 after 30 days of infection has a positive correlation with the increase of IFN-γ and TNF-α in the intestine. However, BMP2 and IFN-γ showed a negative correlation with the number of neurons in the myenteric plexus in the same period in the organ. As a first report of the alteration of BMP2 production after infection by T. cruzi, it is suggested that this imbalance may represent a new pathway in maintaining the intestinal pro-inflammatory profile, as well as being related to the neuronal damage that the infectious process establishes.