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Deinococcus radiodurans R1 Lysate Induces Tolerogenic Maturation in Lipopolysaccharide-Stimulated Dendritic Cells and Protects Dextran Sulfate Sodium-Induced Colitis in Mice

Deinococcus radiodurans is an extremophilic bacterium that can thrive in harsh environments. This property can be attributed to its unique metabolites that possess strong antioxidants and other pharmacological properties. To determine the potential of D. radiodurans R1 lysate (DeinoLys) as a pharmac...

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Autores principales: Song, Ha-Yeon, Han, Jeong Moo, Kim, Woo Sik, Lee, Ji Hee, Park, Woo Yong, Byun, Eui-Baek, Byun, Eui-Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society for Microbiology and Biotechnology 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9628914/
https://www.ncbi.nlm.nih.gov/pubmed/35719091
http://dx.doi.org/10.4014/jmb.2203.03008
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author Song, Ha-Yeon
Han, Jeong Moo
Kim, Woo Sik
Lee, Ji Hee
Park, Woo Yong
Byun, Eui-Baek
Byun, Eui-Hong
author_facet Song, Ha-Yeon
Han, Jeong Moo
Kim, Woo Sik
Lee, Ji Hee
Park, Woo Yong
Byun, Eui-Baek
Byun, Eui-Hong
author_sort Song, Ha-Yeon
collection PubMed
description Deinococcus radiodurans is an extremophilic bacterium that can thrive in harsh environments. This property can be attributed to its unique metabolites that possess strong antioxidants and other pharmacological properties. To determine the potential of D. radiodurans R1 lysate (DeinoLys) as a pharmacological candidate for inflammatory bowel disease (IBD), we investigated the anti-inflammatory activity of DeinoLys in bone marrow-derived dendritic cells (BMDCs) and a colitis mice model. Lipopolysaccharide (LPS)-stimulated BMDCs treated with DeinoLys exhibited alterations in their phenotypic and functional properties by changing into tolerogenic DCs, including strongly inhibited proinflammatory cytokines (TNF-α and IL-12p70) and surface molecule expression and activated DC-induced T cell proliferation/activation with high IL-10 production. These phenotypic and functional changes in BMDCs induced by DeinoLys in the presence of LPS were abrogated by IL-10 neutralization. Furthermore, oral administration of DeinoLys significantly reduced clinical symptoms against dextran sulfate sodium-induced colitis, including body weight loss, disease activity index, histological severity in colon tissue, and lower myeloperoxidase level in mice. Our results establish DeinoLys as a potential anti-inflammatory candidate for IBD therapy.
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spelling pubmed-96289142022-12-13 Deinococcus radiodurans R1 Lysate Induces Tolerogenic Maturation in Lipopolysaccharide-Stimulated Dendritic Cells and Protects Dextran Sulfate Sodium-Induced Colitis in Mice Song, Ha-Yeon Han, Jeong Moo Kim, Woo Sik Lee, Ji Hee Park, Woo Yong Byun, Eui-Baek Byun, Eui-Hong J Microbiol Biotechnol Research article Deinococcus radiodurans is an extremophilic bacterium that can thrive in harsh environments. This property can be attributed to its unique metabolites that possess strong antioxidants and other pharmacological properties. To determine the potential of D. radiodurans R1 lysate (DeinoLys) as a pharmacological candidate for inflammatory bowel disease (IBD), we investigated the anti-inflammatory activity of DeinoLys in bone marrow-derived dendritic cells (BMDCs) and a colitis mice model. Lipopolysaccharide (LPS)-stimulated BMDCs treated with DeinoLys exhibited alterations in their phenotypic and functional properties by changing into tolerogenic DCs, including strongly inhibited proinflammatory cytokines (TNF-α and IL-12p70) and surface molecule expression and activated DC-induced T cell proliferation/activation with high IL-10 production. These phenotypic and functional changes in BMDCs induced by DeinoLys in the presence of LPS were abrogated by IL-10 neutralization. Furthermore, oral administration of DeinoLys significantly reduced clinical symptoms against dextran sulfate sodium-induced colitis, including body weight loss, disease activity index, histological severity in colon tissue, and lower myeloperoxidase level in mice. Our results establish DeinoLys as a potential anti-inflammatory candidate for IBD therapy. The Korean Society for Microbiology and Biotechnology 2022-07-28 2022-06-07 /pmc/articles/PMC9628914/ /pubmed/35719091 http://dx.doi.org/10.4014/jmb.2203.03008 Text en Copyright © 2022 by the authors. Licensee KMB. https://creativecommons.org/licenses/by/4.0/This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Research article
Song, Ha-Yeon
Han, Jeong Moo
Kim, Woo Sik
Lee, Ji Hee
Park, Woo Yong
Byun, Eui-Baek
Byun, Eui-Hong
Deinococcus radiodurans R1 Lysate Induces Tolerogenic Maturation in Lipopolysaccharide-Stimulated Dendritic Cells and Protects Dextran Sulfate Sodium-Induced Colitis in Mice
title Deinococcus radiodurans R1 Lysate Induces Tolerogenic Maturation in Lipopolysaccharide-Stimulated Dendritic Cells and Protects Dextran Sulfate Sodium-Induced Colitis in Mice
title_full Deinococcus radiodurans R1 Lysate Induces Tolerogenic Maturation in Lipopolysaccharide-Stimulated Dendritic Cells and Protects Dextran Sulfate Sodium-Induced Colitis in Mice
title_fullStr Deinococcus radiodurans R1 Lysate Induces Tolerogenic Maturation in Lipopolysaccharide-Stimulated Dendritic Cells and Protects Dextran Sulfate Sodium-Induced Colitis in Mice
title_full_unstemmed Deinococcus radiodurans R1 Lysate Induces Tolerogenic Maturation in Lipopolysaccharide-Stimulated Dendritic Cells and Protects Dextran Sulfate Sodium-Induced Colitis in Mice
title_short Deinococcus radiodurans R1 Lysate Induces Tolerogenic Maturation in Lipopolysaccharide-Stimulated Dendritic Cells and Protects Dextran Sulfate Sodium-Induced Colitis in Mice
title_sort deinococcus radiodurans r1 lysate induces tolerogenic maturation in lipopolysaccharide-stimulated dendritic cells and protects dextran sulfate sodium-induced colitis in mice
topic Research article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9628914/
https://www.ncbi.nlm.nih.gov/pubmed/35719091
http://dx.doi.org/10.4014/jmb.2203.03008
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