Journal of the science of food and agriculture · 2026
Oral PHGG ameliorates atopic dermatitis-like dermatitis with concurrent modulation of colonic IgA and cecal microbiota: implications for the gut-skin axis.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Kakooza Derrick, Yu Hyeonjun, Jeong Jonghyun, Shin Jung Cheul, Kim Woo Jung, Moon Sung-Kwon, Kim Hoon
Аннотация
BACKGROUND: Atopic dermatitis (AD) is increasingly recognized as a systemic inflammatory disorder linked to intestinal immune and microbiome dysregulation. However, whether dietary galactomannan fibers can mitigate AD through coordinated modulation of the gut-skin axis remains unexplored. This study investigated the anti-atopic potential of orally administered partially hydrolyzed guar gum (PHGG), a low-viscosity, fermentable galactomannan enriched in low-mass oligosaccharides (mannose/galactose ratio of 1.87).
RESULTS: In TNF-α/IFN-γ-stimulated HaCaT keratinocytes, PHGG (100-400 μg mL-1) suppressed IL-6, IL-8, and MCP-1 secretion and down-regulated AD-relevant mediators, including TARC, MDC, RANTES, and TSLP. In TNF-α-challenged Caco-2 cells, PHGG reduced IL-8 and MCP-1 and partially restored barrier-associated transcripts (TJP1, TJP2, OCLN, CLDN1) and MUC2. In 2,4-dinitrochlorobenzene (DNCB)-induced AD BALB/c mice, oral PHGG (100-400 mg kg-1 d-1) attenuated lesion severity, epidermal hyperplasia, collagen loss, and mast cell infiltration without adverse effects on body weight or organ weights. PHGG reduced circulating immunoglobulins and inflammatory cytokines, suppressed skin type 2 helper T-cell (Th2)-associated mediators, and restored colonic immune homeostasis, as evidenced by increased immunoglobulin A (IgA) and decreased interleukin 1 beta (IL-1β) and IL-6. Cecal 16S rRNA profiling revealed that PHGG shifted dysbiotic microbial signatures toward fiber-responsive Bacteroidales lineages (e.g., Muribaculaceae, Alistipes, Rikenellaceae) and partially normalized community structure in beta-diversity analyses.
CONCLUSION: These findings demonstrate that oligosaccharide-enriched PHGG ameliorates AD-like inflammation through concurrent modulation of cutaneous immune responses, colonic mucosal immunity, and gut microbial community structure, supporting a gut-skin axis mechanism. Future studies quantifying microbial metabolites are warranted to establish causal mediators of gut-to-skin signaling. © 2026 The Author(s). Journal of the Science of Food and Agriculture published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.
RESULTS: In TNF-α/IFN-γ-stimulated HaCaT keratinocytes, PHGG (100-400 μg mL-1) suppressed IL-6, IL-8, and MCP-1 secretion and down-regulated AD-relevant mediators, including TARC, MDC, RANTES, and TSLP. In TNF-α-challenged Caco-2 cells, PHGG reduced IL-8 and MCP-1 and partially restored barrier-associated transcripts (TJP1, TJP2, OCLN, CLDN1) and MUC2. In 2,4-dinitrochlorobenzene (DNCB)-induced AD BALB/c mice, oral PHGG (100-400 mg kg-1 d-1) attenuated lesion severity, epidermal hyperplasia, collagen loss, and mast cell infiltration without adverse effects on body weight or organ weights. PHGG reduced circulating immunoglobulins and inflammatory cytokines, suppressed skin type 2 helper T-cell (Th2)-associated mediators, and restored colonic immune homeostasis, as evidenced by increased immunoglobulin A (IgA) and decreased interleukin 1 beta (IL-1β) and IL-6. Cecal 16S rRNA profiling revealed that PHGG shifted dysbiotic microbial signatures toward fiber-responsive Bacteroidales lineages (e.g., Muribaculaceae, Alistipes, Rikenellaceae) and partially normalized community structure in beta-diversity analyses.
CONCLUSION: These findings demonstrate that oligosaccharide-enriched PHGG ameliorates AD-like inflammation through concurrent modulation of cutaneous immune responses, colonic mucosal immunity, and gut microbial community structure, supporting a gut-skin axis mechanism. Future studies quantifying microbial metabolites are warranted to establish causal mediators of gut-to-skin signaling. © 2026 The Author(s). Journal of the Science of Food and Agriculture published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.