Effects of zinc deficient diet on development of atopic dermatitis-like eruptions in DS-Nh mice. J Dermatol Sci

Department of Environmental Immuno-Dermatology, Yokohama City University Graduate School of Medicine, Kanagawa, Japan.
Journal of Dermatological Science (Impact Factor: 3.42). 05/2008; 50(1):31-9. DOI: 10.1016/j.jdermsci.2007.11.002
Source: PubMed


Zinc is one of the essential dietary factors and zinc deficiency diminishes the immune system. However, the mechanisms by which zinc deficiency affects the immune system are not fully understood.
We analyzed the mechanisms of zinc deficiency affecting the allergic response using a DS-Nh mouse model of atopic dermatitis.
Male DS-Nh mice were fed a zinc deficient diet for 4 weeks. We measured transepidermal water loss (TEWL) and epidermal moisture level, assessed the skin eruption score, and examined the frequency of lymphocyte subpopulation in spleen and thymus by flow cytometry. The suppressive effect of CD25+CD4+ T cells was analyzed in vitro. The amount of cytokines produced by the spleen cells and the serum IgE levels were measured by ELISA.
In DS-Nh mice fed the zinc deficient diet, skin eruptions were exacerbated and serum IgE levels and number of S. aureus on the skin surface was increased. IFN-gamma and IL-13 production by spleen cells was increased. The number of CD25+CD4+ T cells in spleen was significantly decreased, while the percentage of Foxp3 positive cells in the CD25+CD4+ T cells was comparable to those of the controls. CD25+CD4+ T cells from mice fed the zinc deficient diet maintained a suppressive function compared with those from the controls.
These findings indicate that zinc deficiency influences the skin barrier system and immune system, and suggests that zinc deficiency acts as an exacerbation factor of atopic dermatitis.

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    • "The coat appears dull and dry. In adult animals, deficiency of this mineral mainly manifests as skin changes (Tielsch et al., 2007; Takahashi et al., 2008), although the clinical syndrome is rare, having been reported primarily in dogs of the breeds Siberian husky, Doberman Pinscher, and bull terrier (Willense, 1995; Wilkinson and Harvey, 1996). This is a case report of a dog with zinc deficiency that showed complete clinical remission in response to zinc supplementation. "
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    ABSTRACT: Zinc is an essential mineral of the diet and deficiency can occur because of dietary insufficiency or genetic abnormalities. Zinc deficiency is characterized by alterations in the immune system and in growth and development, as well as lesions in the gastrointestinal system and skin. A male mixed breed dog, 8 years of age, was presented at the veterinary hospital with clinical signs compatible with zinc deficiency. The animal received supplementation with zinc with methionine, and complete resolution was achieved. This paper reports a case of zinc deficiency in a mixed breed dog.
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    • "Minerals, are essential nutrients for human, can trigger alterations on gene expression by initiating signaling events upstream of gene transactivation. Until the present, there are few studies for minerals and AD in human, however, the studies of mice reported that Staphylococcus aureus was increased on the skin of zinc-deficient mice before the development of AD-like eruptions, leading the authors to postulate that zinc may have an important role in the induction of dermatitis [33]. The deficiency of magnesium also induced AD-like skin lesions [34]. "
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    ABSTRACT: Background Mineral water from deep-sea bedrock, formed over thousands of years, is rich in minerals such as Ca, Mg, Na, K, Fe and others. Our present study was to investigate the preventive effects of natural deep-sea water on developing atopic dermatitis (AD). Methods We elicited AD by application of DNCB (2,4-dinitro-chlorobezene) in Nc/Nga mouse dorsal skin. Deep Sea water (DSW) was filtered and concentrated by a nanofiltration process and reverse osmosis. We applied concentrated DSW (CDSW) to lesions five times per week for six weeks, followed by evaluation. 1% pimecrolimus ointment was used as positive control. The severity of skin lesions was assessed macroscopically and histologically. Levels of inflammatory mediators and cytokines in the serum were detected by Enzyme-linked immunosorbent assay (ELISA) and the levels of CD4+ and CD8+ spleen lymphocytes were determined by flow cytometry analysis. Results DNCB-treated mice showed atopic dermatitis-like skin lesions. Treatment of mice with CDSW reduced the severity of symptoms in the skin lesions, including edema, erythema, dryness, itching, and transepidermal water loss (TEWL). Histological analyses demonstrated that epidermal thickness and infiltration of inflammatory cells were decreased after CDSW treatment. Given these interesting observations, we further evaluated the effect of CDSW on immune responses in this AD model. Treatment AD mice with CDSW inhibited up-regulation of IgE, histamine, and pro-inflammatory cytokines in the serum. Also, the CD4+/CD8+ ratio in spleen lymphocyte was down-regulated after treatment with CDSW. Finally, cytokines, especially IL-4 and IL-10 which are important for Th2 cell development, were reduced. Conclusions Our data suggests that topical application of CDSW could be useful in preventing the development of atopic dermatitis.
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