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Single Donor FMT Reverses Microbial/Immune Dysbiosis and Induces Clinical Remission in a Rat Model of Acute Colitis
Deviation in the gut microbial composition is involved in various pathologies, including inflammatory bowel disease (IBD). Faecal microbiota transplant (FMT) can act as a promising approach to treat IBD by which changes in microbiome can be reversed and homeostasis restored. Therefore, the aim of th...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7913212/ https://www.ncbi.nlm.nih.gov/pubmed/33540919 http://dx.doi.org/10.3390/pathogens10020152 |
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author | Adamkova, Petra Hradicka, Petra Gancarcikova, Sona Kassayova, Monika Ambro, Lubos Bertkova, Izabela Maronek, Martin Farkasova Iannaccone, Silvia Demeckova, Vlasta |
author_facet | Adamkova, Petra Hradicka, Petra Gancarcikova, Sona Kassayova, Monika Ambro, Lubos Bertkova, Izabela Maronek, Martin Farkasova Iannaccone, Silvia Demeckova, Vlasta |
author_sort | Adamkova, Petra |
collection | PubMed |
description | Deviation in the gut microbial composition is involved in various pathologies, including inflammatory bowel disease (IBD). Faecal microbiota transplant (FMT) can act as a promising approach to treat IBD by which changes in microbiome can be reversed and homeostasis restored. Therefore, the aim of this study was to investigate the effect of FMT on the remission of acute inflammatory response using dextran sulfate sodium (DSS)-induced rat colitis model. Faecal microbial communities were analysed using the 16S rRNA approach, and clinical manifestations together with histological/haematological/biochemical/immunological analyses were assessed. Our study demonstrated significant shifts in the dominant species of microbiota under inflammatory conditions induced by DSS and evident restoration effect of FMT treatment on microbial composition. These faecal microbial alterations in FMT-treated rats led to a relative restoration of colon length, and a significant decrease in both epithelium damage and disease severity, which was reflected in lower serum pro-inflammatory cytokine levels. Haematological/biochemical parameters in DSS-treated animals showed signs of anaemia with a significant reduction in red blood cell count together with increasing levels of total bilirubin, creatinine and phosphorus suggesting potential protective effect of FMT. These results support FMT as a valuable therapeutic strategy to control inflammation during acute colitis. |
format | Online Article Text |
id | pubmed-7913212 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-79132122021-02-28 Single Donor FMT Reverses Microbial/Immune Dysbiosis and Induces Clinical Remission in a Rat Model of Acute Colitis Adamkova, Petra Hradicka, Petra Gancarcikova, Sona Kassayova, Monika Ambro, Lubos Bertkova, Izabela Maronek, Martin Farkasova Iannaccone, Silvia Demeckova, Vlasta Pathogens Article Deviation in the gut microbial composition is involved in various pathologies, including inflammatory bowel disease (IBD). Faecal microbiota transplant (FMT) can act as a promising approach to treat IBD by which changes in microbiome can be reversed and homeostasis restored. Therefore, the aim of this study was to investigate the effect of FMT on the remission of acute inflammatory response using dextran sulfate sodium (DSS)-induced rat colitis model. Faecal microbial communities were analysed using the 16S rRNA approach, and clinical manifestations together with histological/haematological/biochemical/immunological analyses were assessed. Our study demonstrated significant shifts in the dominant species of microbiota under inflammatory conditions induced by DSS and evident restoration effect of FMT treatment on microbial composition. These faecal microbial alterations in FMT-treated rats led to a relative restoration of colon length, and a significant decrease in both epithelium damage and disease severity, which was reflected in lower serum pro-inflammatory cytokine levels. Haematological/biochemical parameters in DSS-treated animals showed signs of anaemia with a significant reduction in red blood cell count together with increasing levels of total bilirubin, creatinine and phosphorus suggesting potential protective effect of FMT. These results support FMT as a valuable therapeutic strategy to control inflammation during acute colitis. MDPI 2021-02-02 /pmc/articles/PMC7913212/ /pubmed/33540919 http://dx.doi.org/10.3390/pathogens10020152 Text en © 2021 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 Adamkova, Petra Hradicka, Petra Gancarcikova, Sona Kassayova, Monika Ambro, Lubos Bertkova, Izabela Maronek, Martin Farkasova Iannaccone, Silvia Demeckova, Vlasta Single Donor FMT Reverses Microbial/Immune Dysbiosis and Induces Clinical Remission in a Rat Model of Acute Colitis |
title | Single Donor FMT Reverses Microbial/Immune Dysbiosis and Induces Clinical Remission in a Rat Model of Acute Colitis |
title_full | Single Donor FMT Reverses Microbial/Immune Dysbiosis and Induces Clinical Remission in a Rat Model of Acute Colitis |
title_fullStr | Single Donor FMT Reverses Microbial/Immune Dysbiosis and Induces Clinical Remission in a Rat Model of Acute Colitis |
title_full_unstemmed | Single Donor FMT Reverses Microbial/Immune Dysbiosis and Induces Clinical Remission in a Rat Model of Acute Colitis |
title_short | Single Donor FMT Reverses Microbial/Immune Dysbiosis and Induces Clinical Remission in a Rat Model of Acute Colitis |
title_sort | single donor fmt reverses microbial/immune dysbiosis and induces clinical remission in a rat model of acute colitis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7913212/ https://www.ncbi.nlm.nih.gov/pubmed/33540919 http://dx.doi.org/10.3390/pathogens10020152 |
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