Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disease in humans. In this study, we evaluated the effects of a mixture (NCM 1921) of omega-3 butter, omega-3 beef tallow oil, omega-3 lard oil, caprylic acid, lauric acid, choline, and Fe on AD in 1-chloro-2,4-dinitrobenzene (DNCB)-treated NC/Nga mice. NCM 1921 significantly ameliorated the macroscopic and microscopic signs and reduced skin thickness and mast cell incorporation in the skin lesions of mice with DNCB-induced AD. Furthermore, it reduced serum immunoglobulin E levels; reduced the number of IgE-producing B cells, peripheral blood mononuclear cells, white blood cells, and differential white blood cells; and increased the number of lymphocytes. NCM 1921 normalized the total cell number in dorsal skin tissue, the axillary lymph node, and spleen following DNCB exposure and reduced the number of CD23+/B220+ cells in the axillary lymph node and CD3+ cells in dorsal skin tissue. Moreover, it reduced the levels of interleukin (IL)-4 and IL-13 but increased the levels of interferon-γ in anti-CD3–stimulated splenocytes. Immunohistofluorescence staining showed that NCM 1921 treatment significantly increased claudin1, filaggrin, and Sirt1 protein expressions in AD skin lesions. These results suggest that NCM 1921 could be a valuable remedy for the treatment of AD.
Highlights
Atopic dermatitis (AD) is a chronic inflammatory disease of the skin
1921; this healing effect was comparable to that achieved with Dex treatment in the positive controls. These results indicate that NCM 1921 could efficiently reverse AD skin lesions
FACS analysis revealed that NCM 1921 decreased the number of IgE-producing cells and CD23+ /B220+ cells in PBMCs (Figure 2B,C). These results indicate that NCM 1921-mediated suppression of IgE production may play a crucial role in the improvement of AD
Summary
Atopic dermatitis (AD) is a chronic inflammatory disease of the skin. It is characterized by eczematous pruritic lesions, elevated levels of allergen-specific immunoglobulin (Ig) E antibodies in the blood, and infiltration of inflammatory cells that produce proallergic cytokines, such as interleukin (IL)-4, IL-15, and IL-13 [1,2]. The worldwide prevalence of AD is approximately 3% in infants, 10%–20%. Genetic and environmental factors contribute to the development of AD, two hypotheses have been suggested to explain the pathogenesis of AD. The immunological hypothesis proposes that AD develops as a result of an imbalance of Th cells [1]. Th2 cells in the acute eczematic form of dermatitis cause an increase in the production of ILs,
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