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Innovative Animal Model of DSS-Induced Ulcerative Colitis in Pseudo Germ-Free Mice

The aim of this study was to investigate the use of a standardized animal model subjected to antibiotic treatment, and the effects of this treatment on the course of dextran sodium sulphate (DSS)-induced colitis in mice. By decontamination with selective antibiotics and observation of pathogenesis o...

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Autores principales: Gancarcikova, Sona, Lauko, Stanislav, Hrckova, Gabriela, Andrejcakova, Zuzana, Hajduckova, Vanda, Madar, Marian, Kolesar Fecskeova, Livia, Mudronova, Dagmar, Mravcova, Kristina, Strkolcova, Gabriela, Nemcova, Radomira, Kacirova, Jana, Staskova, Andrea, Vilcek, Stefan, Bomba, Alojz
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7761014/
https://www.ncbi.nlm.nih.gov/pubmed/33271873
http://dx.doi.org/10.3390/cells9122571
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author Gancarcikova, Sona
Lauko, Stanislav
Hrckova, Gabriela
Andrejcakova, Zuzana
Hajduckova, Vanda
Madar, Marian
Kolesar Fecskeova, Livia
Mudronova, Dagmar
Mravcova, Kristina
Strkolcova, Gabriela
Nemcova, Radomira
Kacirova, Jana
Staskova, Andrea
Vilcek, Stefan
Bomba, Alojz
author_facet Gancarcikova, Sona
Lauko, Stanislav
Hrckova, Gabriela
Andrejcakova, Zuzana
Hajduckova, Vanda
Madar, Marian
Kolesar Fecskeova, Livia
Mudronova, Dagmar
Mravcova, Kristina
Strkolcova, Gabriela
Nemcova, Radomira
Kacirova, Jana
Staskova, Andrea
Vilcek, Stefan
Bomba, Alojz
author_sort Gancarcikova, Sona
collection PubMed
description The aim of this study was to investigate the use of a standardized animal model subjected to antibiotic treatment, and the effects of this treatment on the course of dextran sodium sulphate (DSS)-induced colitis in mice. By decontamination with selective antibiotics and observation of pathogenesis of ulcerative colitis (UC) induced chemically by exposure of mice to various concentrations of DSS, we obtained an optimum animal PGF model of acute UC manifested by mucin depletion, epithelial degeneration and necrosis, leading to the disappearance of epithelial cells, infiltration of lamina propria and submucosa with neutrophils, cryptitis, and accompanied by decreased viability of intestinal microbiota, loss of body weight, dehydration, moderate rectal bleeding, and a decrease in the selected markers of cellular proliferation and apoptosis. The obtained PGF model did not exhibit changes that could contribute to inflammation by means of alteration of the metabolic status and the induced dysbiosis did not serve as a bearer of pathogenic microorganisms participating in development of ulcerative colitis. The inflammatory process was induced particularly by exposure to DSS and its toxic action on compactness and integrity of mucosal barrier in the large intestine. This offers new possibilities of the use of this animal model in studies with or without participation of pathogenic microbiota in IBD pathogenesis.
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spelling pubmed-77610142020-12-26 Innovative Animal Model of DSS-Induced Ulcerative Colitis in Pseudo Germ-Free Mice Gancarcikova, Sona Lauko, Stanislav Hrckova, Gabriela Andrejcakova, Zuzana Hajduckova, Vanda Madar, Marian Kolesar Fecskeova, Livia Mudronova, Dagmar Mravcova, Kristina Strkolcova, Gabriela Nemcova, Radomira Kacirova, Jana Staskova, Andrea Vilcek, Stefan Bomba, Alojz Cells Article The aim of this study was to investigate the use of a standardized animal model subjected to antibiotic treatment, and the effects of this treatment on the course of dextran sodium sulphate (DSS)-induced colitis in mice. By decontamination with selective antibiotics and observation of pathogenesis of ulcerative colitis (UC) induced chemically by exposure of mice to various concentrations of DSS, we obtained an optimum animal PGF model of acute UC manifested by mucin depletion, epithelial degeneration and necrosis, leading to the disappearance of epithelial cells, infiltration of lamina propria and submucosa with neutrophils, cryptitis, and accompanied by decreased viability of intestinal microbiota, loss of body weight, dehydration, moderate rectal bleeding, and a decrease in the selected markers of cellular proliferation and apoptosis. The obtained PGF model did not exhibit changes that could contribute to inflammation by means of alteration of the metabolic status and the induced dysbiosis did not serve as a bearer of pathogenic microorganisms participating in development of ulcerative colitis. The inflammatory process was induced particularly by exposure to DSS and its toxic action on compactness and integrity of mucosal barrier in the large intestine. This offers new possibilities of the use of this animal model in studies with or without participation of pathogenic microbiota in IBD pathogenesis. MDPI 2020-12-01 /pmc/articles/PMC7761014/ /pubmed/33271873 http://dx.doi.org/10.3390/cells9122571 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Gancarcikova, Sona
Lauko, Stanislav
Hrckova, Gabriela
Andrejcakova, Zuzana
Hajduckova, Vanda
Madar, Marian
Kolesar Fecskeova, Livia
Mudronova, Dagmar
Mravcova, Kristina
Strkolcova, Gabriela
Nemcova, Radomira
Kacirova, Jana
Staskova, Andrea
Vilcek, Stefan
Bomba, Alojz
Innovative Animal Model of DSS-Induced Ulcerative Colitis in Pseudo Germ-Free Mice
title Innovative Animal Model of DSS-Induced Ulcerative Colitis in Pseudo Germ-Free Mice
title_full Innovative Animal Model of DSS-Induced Ulcerative Colitis in Pseudo Germ-Free Mice
title_fullStr Innovative Animal Model of DSS-Induced Ulcerative Colitis in Pseudo Germ-Free Mice
title_full_unstemmed Innovative Animal Model of DSS-Induced Ulcerative Colitis in Pseudo Germ-Free Mice
title_short Innovative Animal Model of DSS-Induced Ulcerative Colitis in Pseudo Germ-Free Mice
title_sort innovative animal model of dss-induced ulcerative colitis in pseudo germ-free mice
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7761014/
https://www.ncbi.nlm.nih.gov/pubmed/33271873
http://dx.doi.org/10.3390/cells9122571
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