Abstract
Recent studies highlighted the T helper (Th)-2 and systemic nature of atopic dermatitis (AD). In addition, gut microbiota is found to be important in the immune development and regulation in AD. Despite the recent biologics evolution, there are still huge unmet needs in the systemic therapies. Oral herbal medicine has been used in the management of AD for centuries in Asia. An oral decaherb (ten herbs) formula is commonly used as an integrative treatment for AD patients in our center. However, its mechanism of action is unknown. We aimed to investigate its mechanism of action and effect on the gut microbiota in mice model with AD. 2,4-dinitrochlorobenzene (DNCB) was applied over the shaved back of mice to induce atopic dermatitis like skin inflammation. A total of 60 female BALB/c mice were randomly divided into positive/negative control groups and low/mid/high dose decaherb groups. Blood and skin biopsy samples were collected on Day 21. Fecal bacterial DNA were sequenced with V4-V5 region of 16S rRNA gene using MiSeq platform. Raw sequence data were analyzed using QIIME2. Histopathological analysis of the lesional skin revealed a decrease in epidermal thickening, eosinophil and mast cell infiltration in dermis in mid/high dose decaherb groups. Serum IgE and CCL17 were lowered in mid/high dose decaherb groups. Level of mRNA expression of Th2 cytokines including interleukin(IL)-4, IL-13, CCL-17 and IL-31 were reduced in the lesional skin of mid/high decaherb groups. Relative abundance of anti-inflammatory short-chain fatty acids (SCFAs) producing bacteria (Ruminococcaceae, Coprococcus and Bifidobacterium) were increased in mid/high dose decaherb groups. This study suggested that oral decaherb formula suppressed the Th2 inflammation and improved the gut microbiota profile in mice model with AD. Further clinical trial is needed to establish and optimize its therapeutic benefit in our AD patients.
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