Modulation of the Gut Microbiota by Sihocheonggan-Tang Shapes the Immune Responses of Atopic Dermatitis

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by complex immune dysregulation and closely related to the gut microbiome. The present study investigated the microbiome-mediated effect of Sihocheonggan-Tang (SHCGT) on AD-like symptoms induced by 2,4-dinitrochlorobenzene (...

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Main Authors: Jaemoo Chun, So Min Lee, You Mee Ahn, Min-Gyung Baek, Hana Yi, Sarah Shin, Jeeyoun Jung
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-09-01
Series:Frontiers in Pharmacology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fphar.2021.722730/full
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author Jaemoo Chun
So Min Lee
You Mee Ahn
Min-Gyung Baek
Min-Gyung Baek
Hana Yi
Sarah Shin
Jeeyoun Jung
author_facet Jaemoo Chun
So Min Lee
You Mee Ahn
Min-Gyung Baek
Min-Gyung Baek
Hana Yi
Sarah Shin
Jeeyoun Jung
author_sort Jaemoo Chun
collection DOAJ
description Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by complex immune dysregulation and closely related to the gut microbiome. The present study investigated the microbiome-mediated effect of Sihocheonggan-Tang (SHCGT) on AD-like symptoms induced by 2,4-dinitrochlorobenzene (DNCB) in BALB/c mice. DNCB was applied regularly to the ear and dorsal skin of BALB/c mice, and SHCGT was administered orally daily for 2 weeks. The composition of the gut microbiota was analyzed using 16S rRNA sequencing, and the effect of gut microbiome-derived metabolites, specifically short-chain fatty acids (SCFAs), was evaluated in tumor necrosis factor-alpha (TNF-α)- and interferon-gamma (IFN-γ)-treated HaCaT cells. SHCGT alleviated DNCB-induced symptoms of AD and the immune response to AD by decreasing the plasma immunoglobulin E level and splenic interleukin-4, interleukin-10, TNF-α, and IFN-γ levels. The gut microbiome composition and the damaged gut epithelial barrier in mice with AD were also significantly altered by SHCGT, and the reduced SCFA levels therein were elevated. We found that SFCAs directly inhibited the mRNA expression of IL-6 and ICAM-1 in TNF-α- and INF-γ-treated HaCaT cells. The finding that SHCGT regulates the gut microbiome and improves DNCB-induced AD in mice suggests that this herbal medicine has therapeutic potential in patients with AD.
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spelling doaj.art-c9036da062554cafb533deeb9d126eda2022-12-21T18:29:25ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122021-09-011210.3389/fphar.2021.722730722730Modulation of the Gut Microbiota by Sihocheonggan-Tang Shapes the Immune Responses of Atopic DermatitisJaemoo Chun0So Min Lee1You Mee Ahn2Min-Gyung Baek3Min-Gyung Baek4Hana Yi5Sarah Shin6Jeeyoun Jung7KM Science Research Division, Korea Institute of Oriental Medicine, Daejeon, South KoreaKM Convergence Research Division, Korea Institute of Oriental Medicine, Daejeon, South KoreaKM Science Research Division, Korea Institute of Oriental Medicine, Daejeon, South KoreaInterdisciplinary Program in Precision Public Health, Korea University, Seoul, South KoreaDepartment of Public Health Sciences, Korea University, Seoul, South KoreaSchool of Biosystems and Biomedical Sciences, Korea University, Seoul, South KoreaKM Science Research Division, Korea Institute of Oriental Medicine, Daejeon, South KoreaKM Science Research Division, Korea Institute of Oriental Medicine, Daejeon, South KoreaAtopic dermatitis (AD) is a chronic inflammatory skin disease characterized by complex immune dysregulation and closely related to the gut microbiome. The present study investigated the microbiome-mediated effect of Sihocheonggan-Tang (SHCGT) on AD-like symptoms induced by 2,4-dinitrochlorobenzene (DNCB) in BALB/c mice. DNCB was applied regularly to the ear and dorsal skin of BALB/c mice, and SHCGT was administered orally daily for 2 weeks. The composition of the gut microbiota was analyzed using 16S rRNA sequencing, and the effect of gut microbiome-derived metabolites, specifically short-chain fatty acids (SCFAs), was evaluated in tumor necrosis factor-alpha (TNF-α)- and interferon-gamma (IFN-γ)-treated HaCaT cells. SHCGT alleviated DNCB-induced symptoms of AD and the immune response to AD by decreasing the plasma immunoglobulin E level and splenic interleukin-4, interleukin-10, TNF-α, and IFN-γ levels. The gut microbiome composition and the damaged gut epithelial barrier in mice with AD were also significantly altered by SHCGT, and the reduced SCFA levels therein were elevated. We found that SFCAs directly inhibited the mRNA expression of IL-6 and ICAM-1 in TNF-α- and INF-γ-treated HaCaT cells. The finding that SHCGT regulates the gut microbiome and improves DNCB-induced AD in mice suggests that this herbal medicine has therapeutic potential in patients with AD.https://www.frontiersin.org/articles/10.3389/fphar.2021.722730/fullSihocheonggan-Tangatopic dermatitisgut microbiomeshort-chain fatty acidsimmune response
spellingShingle Jaemoo Chun
So Min Lee
You Mee Ahn
Min-Gyung Baek
Min-Gyung Baek
Hana Yi
Sarah Shin
Jeeyoun Jung
Modulation of the Gut Microbiota by Sihocheonggan-Tang Shapes the Immune Responses of Atopic Dermatitis
Frontiers in Pharmacology
Sihocheonggan-Tang
atopic dermatitis
gut microbiome
short-chain fatty acids
immune response
title Modulation of the Gut Microbiota by Sihocheonggan-Tang Shapes the Immune Responses of Atopic Dermatitis
title_full Modulation of the Gut Microbiota by Sihocheonggan-Tang Shapes the Immune Responses of Atopic Dermatitis
title_fullStr Modulation of the Gut Microbiota by Sihocheonggan-Tang Shapes the Immune Responses of Atopic Dermatitis
title_full_unstemmed Modulation of the Gut Microbiota by Sihocheonggan-Tang Shapes the Immune Responses of Atopic Dermatitis
title_short Modulation of the Gut Microbiota by Sihocheonggan-Tang Shapes the Immune Responses of Atopic Dermatitis
title_sort modulation of the gut microbiota by sihocheonggan tang shapes the immune responses of atopic dermatitis
topic Sihocheonggan-Tang
atopic dermatitis
gut microbiome
short-chain fatty acids
immune response
url https://www.frontiersin.org/articles/10.3389/fphar.2021.722730/full
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