What question did this study set out to answer?

This research aims to explore how PHGG affects atopic dermatitis and its relationship with gut health.

April 29, 2026Journal of the Science of Food and Agriculture0 citationsOpen Access

Oral PHGG ameliorates atopic dermatitis‐like dermatitis with concurrent modulation of colonic IgA and cecal microbiota: implications for the gut–skin axis

DKDerrick KakoozaInstitute of Science and Technology HYHyeonjun YuKorea University JJJonghyun JeongSeoul National University

Key Points

This research aims to explore how PHGG affects atopic dermatitis and its relationship with gut health.
Administered orally PHGG to evaluate its effects on atopic dermatitis-like symptoms and immune response.
Measured severity of skin lesions, immune markers, and microbiota composition.
Conducted beta-diversity analyses on gut microbiota samples to assess community structure.
PHGG significantly reduced skin lesion severity and inflammation.
Decreased levels of inflammatory cytokines and increased immunoglobulin A were observed.
PHGG shifted gut microbiota toward beneficial Bacteroidales lineages.

Abstract

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: ) 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.

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