Abstract
BackgroundAllergic skin inflammation such as atopic dermatitis (AD), which is characterized by pruritus and inflammation, is regulated partly through the activity of regulatory T cells (Tregs). Tregs play key roles in the immune response by preventing or suppressing the differentiation, proliferation and function of various immune cells, including CD4+ T cells. Recent studies report that fermentation has a tremendous capacity to transform chemical structures or create new substances, and the omega-3 polyunsaturated fatty acids (n-3 PUFAs) in fish oil can reduce inflammation in allergic patients. The beneficial effects of natural fish oil (NFO) have been described in many diseases, but the mechanism by which fermented fish oil (FFO) modulates the immune system and the allergic response is poorly understood. In this study, we produced FFO and tested its ability to suppress the allergic inflammatory response and to activate CD4+CD25+Foxp3+ Tregs.ResultsThe ability of FFO and NFO to modulate the immune system was investigated using a mouse model of AD. Administration of FFO or NFO in the drinking water alleviated the allergic inflammation in the skin, and FFO was more effective than NFO. FFO treatment did increase the expression of the immune-suppressive cytokines TGF-β and IL-10. In addition, ingestion of FFO increased Foxp3 expression and the number of CD4+CD25+Foxp3+ Tregs compared with NFO.ConclusionsThese results suggest that the anti-allergic effect of FFO is associated with enrichment of CD4+CD25+ Foxp3+ T cells at the inflamed sites and that FFO may be effective in treating the allergic symptoms of AD.
Highlights
Allergic skin inflammation such as atopic dermatitis (AD), which is characterized by pruritus and inflammation, is regulated partly through the activity of regulatory T cells (Tregs)
We tested whether fermented fish oil (FFO) or natural fish oil (NFO) has a therapeutic effect on pruritus
Increased TGF-β and forkhead box protein 3 (Foxp3) at sites of inflammation was associated with elevated CD4+CD25+Foxp3+ Treg populations, which can down-regulate the progression of experimental immune disorders
Summary
Allergic skin inflammation such as atopic dermatitis (AD), which is characterized by pruritus and inflammation, is regulated partly through the activity of regulatory T cells (Tregs). Atopic dermatitis (AD), a chronic inflammatory skin disease associated with cutaneous hyper-reactivity, affects approximately 3% of infants, 10 ~ 20% of children and 1 ~ 3% of adults worldwide [1] This systemic disorder is caused by skin barrier dysfunction, severe skin dehydration, and mutations in the filaggrin gene, which has an essential role in modulating epidermal homeostasis. Activated mast cells release a variety of inflammatory mediators following cross-linking of immunoglobulin E (IgE)-receptor complexes at the high-affinity IgE receptor I (FcERI). Of these mediators, histamine is generally considered as a marker of mast cell degranulation in immediate allergic reaction and is a violent inducer of itching. Histamine is a characteristic major mediator in mast cell storage granules and directly triggers type I allergic responses [6,7,8,9,10]
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