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Escherichia coli promotes DSS-induced murine colitis recovery through activation of the TLR4/NF-κB signaling pathway

Increasing evidence suggests that intestinal microbiota have critical function in the pathogenesis of inflammatory bowel disease. This present study investigated the effects of Escherichia coli (E. coli) in mice with dextran sulfate sodium (DSS)-induced colitis. Furthermore, Toll-like receptor 4 (TL...

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Autores principales: Lu, Jiabao, Dong, Boye, Chen, Ailan, He, Feng, Peng, Baifu, Wu, Zixin, Cao, Jie, Li, Wanglin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6390074/
https://www.ncbi.nlm.nih.gov/pubmed/30664156
http://dx.doi.org/10.3892/mmr.2019.9848
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author Lu, Jiabao
Dong, Boye
Chen, Ailan
He, Feng
Peng, Baifu
Wu, Zixin
Cao, Jie
Li, Wanglin
author_facet Lu, Jiabao
Dong, Boye
Chen, Ailan
He, Feng
Peng, Baifu
Wu, Zixin
Cao, Jie
Li, Wanglin
author_sort Lu, Jiabao
collection PubMed
description Increasing evidence suggests that intestinal microbiota have critical function in the pathogenesis of inflammatory bowel disease. This present study investigated the effects of Escherichia coli (E. coli) in mice with dextran sulfate sodium (DSS)-induced colitis. Furthermore, Toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) gene expression was measured by reverse transcription-quantitative polymerase chain reaction. In total, two experiments were performed. In the first experiment, four groups were established in BALB/c mice: i) Group A, control (no treatments); ii) group B, DSS-induced colitis; iii) group C, DSS-induced colitis bacteria depleted (BD) mice; and iv) group D, E. coli-treated DSS-induced colitis BD mice. In the second experiment, there were three groups: i) Group A1, control C57BL/6 mice; ii) group B1, E. coli-treated DSS-induced colitis BD C57BL/6 mice; and iii) E. coli-treated DSS-induced colitis BD TLR4(−/−) mice. Clinical outcomes, colon and immune histopathology and tissue myeloperoxidase activity were assessed. Mice with DSS-induced colitis that were treated with E. coli exhibited enhanced recovery, with significantly improved clinical and histological scores compared with the DSS only group. The mRNA expression of TLR4 and NF-κB in the E. coli-treated group was also significantly higher. These effects were abolished in TLR4(−/−) mice, suggesting that E. coli may have promoted recovery through the TLR4 pathway. The present study indicated that E. coli promoted recovery from DSS-induced colitis in mice, potentially through activation of the TLR4/NF-κB signaling pathway.
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spelling pubmed-63900742019-03-07 Escherichia coli promotes DSS-induced murine colitis recovery through activation of the TLR4/NF-κB signaling pathway Lu, Jiabao Dong, Boye Chen, Ailan He, Feng Peng, Baifu Wu, Zixin Cao, Jie Li, Wanglin Mol Med Rep Articles Increasing evidence suggests that intestinal microbiota have critical function in the pathogenesis of inflammatory bowel disease. This present study investigated the effects of Escherichia coli (E. coli) in mice with dextran sulfate sodium (DSS)-induced colitis. Furthermore, Toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) gene expression was measured by reverse transcription-quantitative polymerase chain reaction. In total, two experiments were performed. In the first experiment, four groups were established in BALB/c mice: i) Group A, control (no treatments); ii) group B, DSS-induced colitis; iii) group C, DSS-induced colitis bacteria depleted (BD) mice; and iv) group D, E. coli-treated DSS-induced colitis BD mice. In the second experiment, there were three groups: i) Group A1, control C57BL/6 mice; ii) group B1, E. coli-treated DSS-induced colitis BD C57BL/6 mice; and iii) E. coli-treated DSS-induced colitis BD TLR4(−/−) mice. Clinical outcomes, colon and immune histopathology and tissue myeloperoxidase activity were assessed. Mice with DSS-induced colitis that were treated with E. coli exhibited enhanced recovery, with significantly improved clinical and histological scores compared with the DSS only group. The mRNA expression of TLR4 and NF-κB in the E. coli-treated group was also significantly higher. These effects were abolished in TLR4(−/−) mice, suggesting that E. coli may have promoted recovery through the TLR4 pathway. The present study indicated that E. coli promoted recovery from DSS-induced colitis in mice, potentially through activation of the TLR4/NF-κB signaling pathway. D.A. Spandidos 2019-03 2019-01-11 /pmc/articles/PMC6390074/ /pubmed/30664156 http://dx.doi.org/10.3892/mmr.2019.9848 Text en Copyright: © Lu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Lu, Jiabao
Dong, Boye
Chen, Ailan
He, Feng
Peng, Baifu
Wu, Zixin
Cao, Jie
Li, Wanglin
Escherichia coli promotes DSS-induced murine colitis recovery through activation of the TLR4/NF-κB signaling pathway
title Escherichia coli promotes DSS-induced murine colitis recovery through activation of the TLR4/NF-κB signaling pathway
title_full Escherichia coli promotes DSS-induced murine colitis recovery through activation of the TLR4/NF-κB signaling pathway
title_fullStr Escherichia coli promotes DSS-induced murine colitis recovery through activation of the TLR4/NF-κB signaling pathway
title_full_unstemmed Escherichia coli promotes DSS-induced murine colitis recovery through activation of the TLR4/NF-κB signaling pathway
title_short Escherichia coli promotes DSS-induced murine colitis recovery through activation of the TLR4/NF-κB signaling pathway
title_sort escherichia coli promotes dss-induced murine colitis recovery through activation of the tlr4/nf-κb signaling pathway
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6390074/
https://www.ncbi.nlm.nih.gov/pubmed/30664156
http://dx.doi.org/10.3892/mmr.2019.9848
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