Correlation between intestinal BMP2, IFNγ, and neural death in experimental infection with Trypanosoma cruzi

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dc.creatorCarmo Neto, José Rodrigues do
dc.creatorSilva, Marcos Vinícius da
dc.creatorBraga, Yarlla Loyane Lira
dc.creatorCosta, Arthur Wilson Florencio da
dc.creatorFonseca, Simone Gonçalves da
dc.creatorNagib, Patricia Resende Alo
dc.creatorCeles, Mara Rúbia Nunes
dc.creatorOliveira, Milton Adriano Pelli
dc.creatorSilva, Juliana Reis Machado e
dc.date.accessioned2025-02-10T12:31:47Z
dc.date.available2025-02-10T12:31:47Z
dc.date.issued2021
dc.description.abstractMegacolon is one of the main late complications of Chagas disease, affecting approximately 10% of symptomatic patients. However, studies are needed to understand the mechanisms involved in the progression of this condition. During infection by Trypanosoma cruzi (T. cruzi), an inflammatory profile sets in that is involved in neural death, and this destruction is known to be essential for megacolon progression. One of the proteins related to the mainte nance of intestinal neurons is the type 2 bone morphogenetic protein (BMP2). Intestinal BMP2 homeostasis is directly involved in the maintenance of organ function. Thus, the aim of this study was to correlate the production of intestinal BMP2 with immunopathological changes in C57Bl/6 mice infected with the T. cruzi Y strain in the acute and chronic phases. The mice were infected with 1000 blood trypomastigote forms. After euthanasia, the colon was collected, divided into two fragments, and a half was used for histological analysis and the other half for BMP2, IFNγ, TNF-α, and IL-10 quantification. The infection induced increased intestinal IFNγ and BMP2 production during the acute phase as well as an increase in the inflammatory infiltrate. In contrast, a decreased number of neurons in the myenteric plexus were observed during this phase. Collagen deposition increased gradually throughout the infection, as demonstrated in the chronic phase. Additionally, a BMP2 increase during the acute phase was positively correlated with intestinal IFNγ. In the same analyzed period, BMP2 and IFNγ showed negative correlations with the number of neurons in the myenteric plexus. As the first report of BMP2 alteration after infection by T. cruzi, we suggest that this imbalance is not only related to neuronal damage but may also represent a new route for maintaining the intestinal proinflammatory profile during the acute phase.
dc.identifier.citationCARMO NETO, José Rodrigues do et al. Correlation between intestinal BMP2, IFNγ, and neural death in experimental infection with Trypanosoma cruzi. Plos One, San Francisco, v. 16, n. 2, e0246692, 2021. DOI: 10.1371/journal.pone.0246692. Disponível em: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0246692. Acesso em: 5 fev. 2025.
dc.identifier.doi10.1371/journal.pone.0246692
dc.identifier.issne- 1932-6203
dc.identifier.urihttp://repositorio.bc.ufg.br//handle/ri/26625
dc.language.isoeng
dc.publisher.countryEstados unidos
dc.publisher.departmentInstituto de Patologia Tropical e Saúde Pública - IPTSP (RMG)
dc.rightsAcesso Aberto
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.titleCorrelation between intestinal BMP2, IFNγ, and neural death in experimental infection with Trypanosoma cruzi
dc.typeArtigo

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