Please use this identifier to cite or link to this item: http://www.repositorio.ufop.br/handle/123456789/6631
Title: Enteric neuronal damage, intramuscular denervation and smooth muscle phenotype changes as mechanisms of chagasic megacolon : evidence from a long - term murine model of Tripanosoma cruzi infection.
Authors: Campos, Camila França
Cangussú, Silvia Dantas
Duz, Ana Luiza Cassin
Cartelle, Christiane Teixeira
Noviello, Maria de Lourdes
Veloso, Vanja Maria
Bahia, Maria Terezinha
Leite, Camila Megale Almeida
Arantes, Rosa Maria Esteves
Issue Date: 2016
Citation: CAMPOS, C. F. et al. Enteric neuronal damage, intramuscular denervation and smooth muscle phenotype changes as mechanisms of chagasic megacolon: evidence from a long - term murine model of Tripanosoma cruzi infection. Plos One, v. 11, p. e0153038, 2016. Disponível em: <http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0153038>. Acesso em: 16 jun. 2016.
Abstract: We developed a novel murine model of long-term infection with Trypanosoma cruzi with the aim to elucidate the pathogenesis of megacolon and the associated adaptive and neuromuscular intestinal disorders. Our intent was to produce a chronic stage of the disease since the early treatment should avoid 100% mortality of untreated animals at acute phase. Treatment allowed animals to be kept infected and alive in order to develop the chronic phase of infection with low parasitism as in human disease. A group of Swiss mice was infected with the Y strain of T. cruzi. At the 11th day after infection, a sub-group was euthanized (acute-phase group) and another sub-group was treated with benznidazole and euthanized 15 months after infection (chronic-phase group). Whole colon samples were harvested and used for studying the histopathology of the intestinal smooth muscle and the plasticity of the enteric nerves. In the acute phase, all animals presented inflammatory lesions associated with intense and diffuse parasitism of the muscular and submucosa layers, which were enlarged when compared with the controls. The occurrence of intense degenerative inflammatory changes and increased reticular fibers suggests inflammatoryinduced necrosis of muscle cells. In the chronic phase, parasitism was insignificant; however, he architecture of Aüerbach plexuses was focally affected in the inflamed areas, and a significant decrease in the number of neurons and in the density of intramuscular nerve bundles was detected. Other changes observed included increased thickness of the colon wall, diffuse muscle cell hypertrophy, and increased collagen deposition, indicating early fibrosis in the damaged areas. Mast cell count significantly increased in the muscular layers. We propose a model for studying the long-term (15 months) pathogenesis of Chagasic megacolon in mice that mimics the human disease, which persists for several years and has not been fully elucidated. We hypothesize that the long-term inflammatory process mediates neuronal damage and intramuscular and intramural denervation, leading to phenotypic changes in smooth muscle cells associated with fibrosis. These long-term structural changes may represent the basic mechanism for the formation of the Chagasic megacolon.
URI: http://www.repositorio.ufop.br/handle/123456789/6631
metadata.dc.identifier.doi: https://doi.org/10.1371/journal.pone.0153038
ISSN: 1932-6203
metadata.dc.rights.license: This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Fonte: o próprio artigo.
Appears in Collections:DECBI - Artigos publicados em periódicos

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