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Colonic motility adjustments in acute and chronic DSS-induced colitis.
da Silva Watanabe, Paulo; Cavichioli, Andreza Manzato; D'Arc de Lima Mendes, Joana; Aktar, Rubina; Peiris, Madusha; Blackshaw, L Ashley; de Almeida Araújo, Eduardo José.
Afiliación
  • da Silva Watanabe P; Department of Histology, State University of Londrina, Londrina, PR, Brazil.
  • Cavichioli AM; Department of Histology, State University of Londrina, Londrina, PR, Brazil.
  • D'Arc de Lima Mendes J; Department of Histology, State University of Londrina, Londrina, PR, Brazil.
  • Aktar R; Wingate Institute for Neurogastroenterology, Centre for Neuroscience, Surgery and Trauma, Blizard Institute, Queen Mary University of London, London, UK.
  • Peiris M; Wingate Institute for Neurogastroenterology, Centre for Neuroscience, Surgery and Trauma, Blizard Institute, Queen Mary University of London, London, UK.
  • Blackshaw LA; Wingate Institute for Neurogastroenterology, Centre for Neuroscience, Surgery and Trauma, Blizard Institute, Queen Mary University of London, London, UK.
  • de Almeida Araújo EJ; Department of Histology, State University of Londrina, Londrina, PR, Brazil. Electronic address: eduardoaraujo@uel.br.
Life Sci ; 321: 121642, 2023 May 15.
Article en En | MEDLINE | ID: mdl-36990176
AIMS: Inflammatory bowel disease is recurrent inflammation that affects the gastrointestinal tract causing changes in intestinal motility. The evolution of these changes is not completely understood. The aim of this study was to evaluate anatomical and functional changes in the colon during the development of acute and chronic DSS-induced ulcerative colitis (UC) in C57Bl/6 mice. MATERIALS AND METHODS: Mice were relocated into 5 groups: control (GC) and groups exposed to DSS 3 % for 2 (DSS2d), 5 (DSS5d) and 7 DSS7d) days (acute UC) or 3 cycles (DSS3C; Chronic UC). Mice were monitored daily. After euthanasia, colonic tissue was assessed with histological, immunofluorescence and colon manometry methods. KEY FINDINGS: Ulcerative Colitis is a chronic disease characterized by overt inflammation of the colon. Here we investigate whether the morphological changes caused by UC in the colonic wall, in tuft cells and in enteric neurons also promote any alteration in colonic motility patterns. UC Promotes thickening in the colonic wall, fibrosis, reduction in the number of tuft cells and consequently goblet cells also, without promoting neuronal death however there is a change in the chemical code of myenteric neurons. All of these morphological changes were responsible for causing a change in colonic contractions, colonic migration motor complex, total time of gastrointestinal transit and therefore promoting dysmotility. Further studies stimulating a hyperplasia of tuft cells may be the way to try to keep the colonic epithelium healthy, reducing the damage caused by UC. SIGNIFICANCE: Increasing disease pathology of DSS-induced UC induces structural and neuroanatomical changes and driven damage to cholinergic neurons causes colonic dysmotility, including increase of cholinergic myenteric neurons, followed by variations in the motility pattern of different regions of the colon that taking together characterize colonic dysmotility.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Colitis Ulcerosa / Colitis Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Life Sci Año: 2023 Tipo del documento: Article País de afiliación: Brasil Pais de publicación: Países Bajos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Colitis Ulcerosa / Colitis Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Life Sci Año: 2023 Tipo del documento: Article País de afiliación: Brasil Pais de publicación: Países Bajos