Topical Administration of a Mixed Microbial Culture of Lactobacillus paracasei, Pichia membranifaciens and Saccharomyces cerevisiae Significantly Inhibits the Development of Atopic Dermatitis in a Mouse Model Through IL-10 Overexpression by Dendritic Cells

局部应用由副干酪乳杆菌、膜状毕赤酵母和酿酒酵母组成的混合微生物培养物,可通过树突状细胞过表达IL-10显著抑制小鼠特应性皮炎的发展。

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Abstract

Background/Objectives: In this study, we focused on a mixed microbial culture of Lactobacillus paracasei, Pichia membranifaciens, and Saccharomyces cerevisiae (LS) as a new probiotic and examined the therapeutic and preventive effects of topical treatment with LS in a mouse model of atopic dermatitis (AD). Methods: Immunomodulatory effects of LS were examined with murine dendritic cell lines (DC2.4) by measuring the interleukin (IL)-10 and tumor necrosis factor (TNF) α levels. The anti-inflammatory effects of LS were evaluated in stimulated human epidermal keratinocytes (HaCaTs) by focusing on the production of IL-8 and thymus and activation-regulated chemokine (TARC). Therapeutic and preventive properties of topical treatment with LS (10%) were finally examined in a mouse model of AD developed by topical sensitization to house dust mite ointment. Clinical symptoms, back skin thickness, and transepidermal water loss (TEWL) were monitored weekly, and the immune responses in the auricular lymph nodes were analyzed after necropsy. Results: LS treatment significantly enhanced the secretions of IL-10 and TNFα by DC2.4 cells. IL-8 and TARC production by stimulated HaCaT cells was significantly decreased by co-culturing with LS. Although there were no significant changes in clinical symptoms, skin thickness, or TEWL in the therapeutic setting of the AD mouse model, the number of IgE-positive B cells and IL-4 levels in the local lymph nodes significantly decreased in the LS treatment group. Preventive treatment with LS significantly decreased AD symptoms compared to those in AD control mice. Conclusions: Our findings indicate that the immunomodulatory and anti-inflammatory effects of LS prevent the development of AD.

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