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Effect of fecal microbiota transplantation on the TGF-β1/Smad signaling pathway in rats with TNBS-induced colitis

BACKGROUND: Traditional treatments for inflammatory bowel disease (IBD) have adverse side effects, and patients who receive such treatments have high recurrence rates. Fecal microbiota transplantation (FMT) has become an increasingly popular therapeutic option for patients with IBD. However, the mec...

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Autores principales: Qiu, Jinlang, Wu, Caixian, Gao, Qianyu, Li, Sheng, Li, Yuhua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9403912/
https://www.ncbi.nlm.nih.gov/pubmed/36034975
http://dx.doi.org/10.21037/atm-22-3227
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author Qiu, Jinlang
Wu, Caixian
Gao, Qianyu
Li, Sheng
Li, Yuhua
author_facet Qiu, Jinlang
Wu, Caixian
Gao, Qianyu
Li, Sheng
Li, Yuhua
author_sort Qiu, Jinlang
collection PubMed
description BACKGROUND: Traditional treatments for inflammatory bowel disease (IBD) have adverse side effects, and patients who receive such treatments have high recurrence rates. Fecal microbiota transplantation (FMT) has become an increasingly popular therapeutic option for patients with IBD. However, the mechanism by which FMT alleviates this disease remains unclear. METHODS: In this study, a rat model of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis was established and used to explore whether the transforming growth factor-beta 1 (TGF-β1)/small mothers against decapentaplegic (Smad) signaling pathway plays a critical role in the FMT alleviation of IBD. RESULTS: After the FMT intervention, the disease activity index and histologic scores were significantly decreased. In addition, the TGF-β1 expression level in the FMT group was significantly decreased by approximately 0.72-fold relative to the level in the TNBS colitis group, whereas the Smad3, Smad4, and Smad7 expression levels had increased by approximately 1.21, 1.40, and 1.18 folds, respectively. Similarly, SB431542 inhibited the expression of TGF-β1 and promoted the expression of Smad3, Smad4, and Smad7. Further, the serum levels of the inflammatory cytokines tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) were significantly decreased, whereas that of the interferon-gamma (IFN-γ) was not significantly changed after the FMT intervention. CONCLUSIONS: These results suggest that FMT inhibits the TGF-β1/Smad signaling pathway to attenuate inflammation.
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spelling pubmed-94039122022-08-26 Effect of fecal microbiota transplantation on the TGF-β1/Smad signaling pathway in rats with TNBS-induced colitis Qiu, Jinlang Wu, Caixian Gao, Qianyu Li, Sheng Li, Yuhua Ann Transl Med Original Article BACKGROUND: Traditional treatments for inflammatory bowel disease (IBD) have adverse side effects, and patients who receive such treatments have high recurrence rates. Fecal microbiota transplantation (FMT) has become an increasingly popular therapeutic option for patients with IBD. However, the mechanism by which FMT alleviates this disease remains unclear. METHODS: In this study, a rat model of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis was established and used to explore whether the transforming growth factor-beta 1 (TGF-β1)/small mothers against decapentaplegic (Smad) signaling pathway plays a critical role in the FMT alleviation of IBD. RESULTS: After the FMT intervention, the disease activity index and histologic scores were significantly decreased. In addition, the TGF-β1 expression level in the FMT group was significantly decreased by approximately 0.72-fold relative to the level in the TNBS colitis group, whereas the Smad3, Smad4, and Smad7 expression levels had increased by approximately 1.21, 1.40, and 1.18 folds, respectively. Similarly, SB431542 inhibited the expression of TGF-β1 and promoted the expression of Smad3, Smad4, and Smad7. Further, the serum levels of the inflammatory cytokines tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) were significantly decreased, whereas that of the interferon-gamma (IFN-γ) was not significantly changed after the FMT intervention. CONCLUSIONS: These results suggest that FMT inhibits the TGF-β1/Smad signaling pathway to attenuate inflammation. AME Publishing Company 2022-08 /pmc/articles/PMC9403912/ /pubmed/36034975 http://dx.doi.org/10.21037/atm-22-3227 Text en 2022 Annals of Translational Medicine. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) .
spellingShingle Original Article
Qiu, Jinlang
Wu, Caixian
Gao, Qianyu
Li, Sheng
Li, Yuhua
Effect of fecal microbiota transplantation on the TGF-β1/Smad signaling pathway in rats with TNBS-induced colitis
title Effect of fecal microbiota transplantation on the TGF-β1/Smad signaling pathway in rats with TNBS-induced colitis
title_full Effect of fecal microbiota transplantation on the TGF-β1/Smad signaling pathway in rats with TNBS-induced colitis
title_fullStr Effect of fecal microbiota transplantation on the TGF-β1/Smad signaling pathway in rats with TNBS-induced colitis
title_full_unstemmed Effect of fecal microbiota transplantation on the TGF-β1/Smad signaling pathway in rats with TNBS-induced colitis
title_short Effect of fecal microbiota transplantation on the TGF-β1/Smad signaling pathway in rats with TNBS-induced colitis
title_sort effect of fecal microbiota transplantation on the tgf-β1/smad signaling pathway in rats with tnbs-induced colitis
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9403912/
https://www.ncbi.nlm.nih.gov/pubmed/36034975
http://dx.doi.org/10.21037/atm-22-3227
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