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Alleviation of DSS-induced colitis in mice by a new-isolated Lactobacillus acidophilus C4

INTRODUCTION: Probiotic is adjuvant therapy for traditional drug treatment of ulcerative colitis (UC). In the present study, Lactobacillus acidophilus C4 with high acid and bile salt resistance has been isolated and screened, and the beneficial effect of L. acidophilus C4 on Dextran Sulfate Sodium (...

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Autores principales: Liu, Qianqian, Jian, Wenwen, Wang, Lu, Yang, Shenglin, Niu, Yutian, Xie, ShuaiJing, Hayer, Kim, Chen, Kun, Zhang, Yi, Guo, Yanan, Tu, Zeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10157218/
https://www.ncbi.nlm.nih.gov/pubmed/37152759
http://dx.doi.org/10.3389/fmicb.2023.1137701
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author Liu, Qianqian
Jian, Wenwen
Wang, Lu
Yang, Shenglin
Niu, Yutian
Xie, ShuaiJing
Hayer, Kim
Chen, Kun
Zhang, Yi
Guo, Yanan
Tu, Zeng
author_facet Liu, Qianqian
Jian, Wenwen
Wang, Lu
Yang, Shenglin
Niu, Yutian
Xie, ShuaiJing
Hayer, Kim
Chen, Kun
Zhang, Yi
Guo, Yanan
Tu, Zeng
author_sort Liu, Qianqian
collection PubMed
description INTRODUCTION: Probiotic is adjuvant therapy for traditional drug treatment of ulcerative colitis (UC). In the present study, Lactobacillus acidophilus C4 with high acid and bile salt resistance has been isolated and screened, and the beneficial effect of L. acidophilus C4 on Dextran Sulfate Sodium (DSS)-induced colitis in mice has been evaluated. Our data showed that oral administration of L. acidophilus C4 remarkably alleviated colitis symptoms in mice and minimized colon tissue damage. METHODS: To elucidate the underlying mechanism, we have investigated the levels of inflammatory cytokines and intestinal tight junction (TJ) related proteins (occludin and ZO-1) in colon tissue, as well as the intestinal microbiota and short-chain fatty acids (SCFAs) in feces. RESULTS: Compared to the DSS group, the inflammatory cytokines IL-1β, IL-6, and TNF-α in L. acidophilus C4 group were reduced, while the antioxidant enzymes superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT) were found to be elevated. In addition, proteins linked to TJ were elevated after L. acidophilus C4 intervention. Further study revealed that L. acidophilus C4 reversed the decrease in intestinal microbiota diversity caused by colitis and promoted the levels of SCFAs. DISCUSSION: This study demonstrate that L. acidophilus C4 effectively alleviated DSS-induced colitis in mice by repairing the mucosal barrier and maintaining the intestinal microecological balance. L. acidophilus C4 could be of great potential for colitis therapy.
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spelling pubmed-101572182023-05-05 Alleviation of DSS-induced colitis in mice by a new-isolated Lactobacillus acidophilus C4 Liu, Qianqian Jian, Wenwen Wang, Lu Yang, Shenglin Niu, Yutian Xie, ShuaiJing Hayer, Kim Chen, Kun Zhang, Yi Guo, Yanan Tu, Zeng Front Microbiol Microbiology INTRODUCTION: Probiotic is adjuvant therapy for traditional drug treatment of ulcerative colitis (UC). In the present study, Lactobacillus acidophilus C4 with high acid and bile salt resistance has been isolated and screened, and the beneficial effect of L. acidophilus C4 on Dextran Sulfate Sodium (DSS)-induced colitis in mice has been evaluated. Our data showed that oral administration of L. acidophilus C4 remarkably alleviated colitis symptoms in mice and minimized colon tissue damage. METHODS: To elucidate the underlying mechanism, we have investigated the levels of inflammatory cytokines and intestinal tight junction (TJ) related proteins (occludin and ZO-1) in colon tissue, as well as the intestinal microbiota and short-chain fatty acids (SCFAs) in feces. RESULTS: Compared to the DSS group, the inflammatory cytokines IL-1β, IL-6, and TNF-α in L. acidophilus C4 group were reduced, while the antioxidant enzymes superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT) were found to be elevated. In addition, proteins linked to TJ were elevated after L. acidophilus C4 intervention. Further study revealed that L. acidophilus C4 reversed the decrease in intestinal microbiota diversity caused by colitis and promoted the levels of SCFAs. DISCUSSION: This study demonstrate that L. acidophilus C4 effectively alleviated DSS-induced colitis in mice by repairing the mucosal barrier and maintaining the intestinal microecological balance. L. acidophilus C4 could be of great potential for colitis therapy. Frontiers Media S.A. 2023-04-20 /pmc/articles/PMC10157218/ /pubmed/37152759 http://dx.doi.org/10.3389/fmicb.2023.1137701 Text en Copyright © 2023 Liu, Jian, Wang, Yang, Niu, Xie, Hayer, Chen, Zhang, Guo and Tu. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Microbiology
Liu, Qianqian
Jian, Wenwen
Wang, Lu
Yang, Shenglin
Niu, Yutian
Xie, ShuaiJing
Hayer, Kim
Chen, Kun
Zhang, Yi
Guo, Yanan
Tu, Zeng
Alleviation of DSS-induced colitis in mice by a new-isolated Lactobacillus acidophilus C4
title Alleviation of DSS-induced colitis in mice by a new-isolated Lactobacillus acidophilus C4
title_full Alleviation of DSS-induced colitis in mice by a new-isolated Lactobacillus acidophilus C4
title_fullStr Alleviation of DSS-induced colitis in mice by a new-isolated Lactobacillus acidophilus C4
title_full_unstemmed Alleviation of DSS-induced colitis in mice by a new-isolated Lactobacillus acidophilus C4
title_short Alleviation of DSS-induced colitis in mice by a new-isolated Lactobacillus acidophilus C4
title_sort alleviation of dss-induced colitis in mice by a new-isolated lactobacillus acidophilus c4
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10157218/
https://www.ncbi.nlm.nih.gov/pubmed/37152759
http://dx.doi.org/10.3389/fmicb.2023.1137701
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