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Galectin-9 Induced by Dietary Prebiotics Regulates Immunomodulation to Reduce Atopic Dermatitis Symptoms in 1-Chloro- 2,4-Dinitrobenzene (DNCB)-Treated NC/Nga Mice

Atopic dermatitis (AD) is a skin disorder that causes chronic itch. We investigated the inhibitory effects of a mixture of prebiotic short-chain galacto-oligosaccharides and long-chain fructo- oligosaccharides (scGOS/lcFOS), inulin, or β-glucan on AD development in 1-chloro-2,4- dinitrobenzene (DNCB...

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Autores principales: Kim, Jeong A, Kim, Sung Hak, Kim, In Sung, Yu, Da Yoon, Kim, Gwang Il, Moon, Yang Soo, Kim, Sung Chan, Lee, Seung Ho, Lee, Sang Suk, Yun, Cheol-Heui, Choi, In Soon, Cho, Kwang Keun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society for Microbiology and Biotechnology 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9745654/
https://www.ncbi.nlm.nih.gov/pubmed/32699202
http://dx.doi.org/10.4014/jmb.2005.05017
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author Kim, Jeong A
Kim, Sung Hak
Kim, In Sung
Yu, Da Yoon
Kim, Gwang Il
Moon, Yang Soo
Kim, Sung Chan
Lee, Seung Ho
Lee, Sang Suk
Yun, Cheol-Heui
Choi, In Soon
Cho, Kwang Keun
author_facet Kim, Jeong A
Kim, Sung Hak
Kim, In Sung
Yu, Da Yoon
Kim, Gwang Il
Moon, Yang Soo
Kim, Sung Chan
Lee, Seung Ho
Lee, Sang Suk
Yun, Cheol-Heui
Choi, In Soon
Cho, Kwang Keun
author_sort Kim, Jeong A
collection PubMed
description Atopic dermatitis (AD) is a skin disorder that causes chronic itch. We investigated the inhibitory effects of a mixture of prebiotic short-chain galacto-oligosaccharides and long-chain fructo- oligosaccharides (scGOS/lcFOS), inulin, or β-glucan on AD development in 1-chloro-2,4- dinitrobenzene (DNCB)-treated NC/Nga mice. Mice were randomly assigned to six groups: untreated mice, AD control, positive control (DNCB-treated NC/Nga mice fed a dietary supplement of Zyrtec), and DNCB-treated NC/Nga mice fed a dietary supplement of prebiotics such as scGOS/lcFOS (T1), inulin (T2), or β-glucan (T3). The prebiotic treatment groups (T1, T2, and T3) showed suppression of AD symptoms, Th2 cell differentiation, and AD-like skin lesions induced by DNCB. In addition, prebiotic treatment also reduced the number of microorganisms such as Firmicutes, which is associated with AD symptoms, and increased the levels of Bacteroidetes and Ruminococcaceae, which are associated with alleviation of AD symptoms. Our findings demonstrate the inhibitory effects of prebiotics on AD development by improving the Th1/Th2 cytokine balance and beneficial symbiotic microorganisms in in vitro and in vivo models.
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spelling pubmed-97456542022-12-13 Galectin-9 Induced by Dietary Prebiotics Regulates Immunomodulation to Reduce Atopic Dermatitis Symptoms in 1-Chloro- 2,4-Dinitrobenzene (DNCB)-Treated NC/Nga Mice Kim, Jeong A Kim, Sung Hak Kim, In Sung Yu, Da Yoon Kim, Gwang Il Moon, Yang Soo Kim, Sung Chan Lee, Seung Ho Lee, Sang Suk Yun, Cheol-Heui Choi, In Soon Cho, Kwang Keun J Microbiol Biotechnol Research article Atopic dermatitis (AD) is a skin disorder that causes chronic itch. We investigated the inhibitory effects of a mixture of prebiotic short-chain galacto-oligosaccharides and long-chain fructo- oligosaccharides (scGOS/lcFOS), inulin, or β-glucan on AD development in 1-chloro-2,4- dinitrobenzene (DNCB)-treated NC/Nga mice. Mice were randomly assigned to six groups: untreated mice, AD control, positive control (DNCB-treated NC/Nga mice fed a dietary supplement of Zyrtec), and DNCB-treated NC/Nga mice fed a dietary supplement of prebiotics such as scGOS/lcFOS (T1), inulin (T2), or β-glucan (T3). The prebiotic treatment groups (T1, T2, and T3) showed suppression of AD symptoms, Th2 cell differentiation, and AD-like skin lesions induced by DNCB. In addition, prebiotic treatment also reduced the number of microorganisms such as Firmicutes, which is associated with AD symptoms, and increased the levels of Bacteroidetes and Ruminococcaceae, which are associated with alleviation of AD symptoms. Our findings demonstrate the inhibitory effects of prebiotics on AD development by improving the Th1/Th2 cytokine balance and beneficial symbiotic microorganisms in in vitro and in vivo models. The Korean Society for Microbiology and Biotechnology 2020-09-28 2020-07-23 /pmc/articles/PMC9745654/ /pubmed/32699202 http://dx.doi.org/10.4014/jmb.2005.05017 Text en Copyright © 2020 The Korean Society for Microbiology and Biotechnology 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
Kim, Jeong A
Kim, Sung Hak
Kim, In Sung
Yu, Da Yoon
Kim, Gwang Il
Moon, Yang Soo
Kim, Sung Chan
Lee, Seung Ho
Lee, Sang Suk
Yun, Cheol-Heui
Choi, In Soon
Cho, Kwang Keun
Galectin-9 Induced by Dietary Prebiotics Regulates Immunomodulation to Reduce Atopic Dermatitis Symptoms in 1-Chloro- 2,4-Dinitrobenzene (DNCB)-Treated NC/Nga Mice
title Galectin-9 Induced by Dietary Prebiotics Regulates Immunomodulation to Reduce Atopic Dermatitis Symptoms in 1-Chloro- 2,4-Dinitrobenzene (DNCB)-Treated NC/Nga Mice
title_full Galectin-9 Induced by Dietary Prebiotics Regulates Immunomodulation to Reduce Atopic Dermatitis Symptoms in 1-Chloro- 2,4-Dinitrobenzene (DNCB)-Treated NC/Nga Mice
title_fullStr Galectin-9 Induced by Dietary Prebiotics Regulates Immunomodulation to Reduce Atopic Dermatitis Symptoms in 1-Chloro- 2,4-Dinitrobenzene (DNCB)-Treated NC/Nga Mice
title_full_unstemmed Galectin-9 Induced by Dietary Prebiotics Regulates Immunomodulation to Reduce Atopic Dermatitis Symptoms in 1-Chloro- 2,4-Dinitrobenzene (DNCB)-Treated NC/Nga Mice
title_short Galectin-9 Induced by Dietary Prebiotics Regulates Immunomodulation to Reduce Atopic Dermatitis Symptoms in 1-Chloro- 2,4-Dinitrobenzene (DNCB)-Treated NC/Nga Mice
title_sort galectin-9 induced by dietary prebiotics regulates immunomodulation to reduce atopic dermatitis symptoms in 1-chloro- 2,4-dinitrobenzene (dncb)-treated nc/nga mice
topic Research article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9745654/
https://www.ncbi.nlm.nih.gov/pubmed/32699202
http://dx.doi.org/10.4014/jmb.2005.05017
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