Abstract
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.
Highlights
Atopic dermatitis (AD) is a chronic inflammatory skin disease caused by immune system dysfunction and environmental stress (Akdis et al, 2000)
We further identified the chemical components of SHCGT based on ultra-performance liquid chromatography (UPLC)-Q-TOF MS analysis
We suggested that SHCGT relieves the atopic dermatitis in a dose-dependent manner, and shortchain fatty acids (SCFAs) produced by intestinal microorganisms changed by SHCGT play a role in improving the atopic dermatitis
Summary
Atopic dermatitis (AD) is a chronic inflammatory skin disease caused by immune system dysfunction and environmental stress (Akdis et al, 2000). It is typically characterized by increases in T helper (Th) 2 cell-mediated inflammatory responses, including the release of immunoglobulin E (IgE), interleukin (IL)-4, IL-5, and IL-13 in the acute phase, whereas an increasing proportion of Th1 cells accounts for the chronic phase of the immune response (Biedermann et al, 2015; Moreno et al, 2016). A new approach is needed to treat AD effectively (Paller et al, 2017)
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