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Heat-Killed Enterococcus faecalis EF-2001 Ameliorates Atopic Dermatitis in a Murine Model

机译:热杀死粪肠球菌EF-2001改善小鼠模型中的特应性皮炎

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摘要

Recent reports have shown the immunomodulatory effect of heat-killed lactic acid bacteria. Atopic dermatitis (AD) is an allergic skin disease, caused by immune dysregulation among other factors. The aim of this study was to assess the effect of heat-killed Enterococcus faecalis EF-2001 (EF-2001) on AD. We established an in vivo AD model by repeated local exposure of Dermatophagoides farinae extract (DFE; house dust mite extract) and 2,4-dinitrochlorobenzene (DNCB) to the ears of mice. After oral administration of EF-2001 for four weeks, the epidermal and dermal ear thickness, mast cell infiltration, and serum immunoglobulin levels were measured. In addition, the gene expression levels of pathogenic cytokines in the ears, lymph nodes, and splenocytes were assayed. EF-2001 attenuated AD symptoms based on the ear thickness, histopathological analysis, and serum immunoglobulin levels. Moreover, EF-2001 decreased the DFE/DNCB-induced expression of various pathogenic cytokines in the ears, lymph nodes, and splenocytes. These results suggest that EF-2001 has therapeutic potential in the treatment of AD owing to its immunomodulatory effects.
机译:最近的报道显示了热杀死的乳酸菌的免疫调节作用。特应性皮炎(AD)是一种过敏性皮肤病,由免疫调节异常等因素引起。这项研究的目的是评估热杀死粪肠球菌EF-2001(EF-2001)对AD的影响。我们通过重复向小鼠的耳朵局部暴露Dermatophagoides farinae提取物(DFE;屋尘螨提取物)和2,4-二硝基氯苯(DNCB),建立了体内AD模型。 EF-2001口服4周后,测量了表皮和真皮耳的厚度,肥大细胞浸润和血清免疫球蛋白水平。另外,测定了在耳朵,淋巴结和脾细胞中的致病细胞因子的基因表达水平。 EF-2001可根据耳朵厚度,组织病理学分析和血清免疫球蛋白水平减轻AD症状。此外,EF-2001降低了DFE / DNCB诱导的耳,淋巴结和脾细胞中各种致病细胞因子的表达。这些结果表明,EF-2001由于其免疫调节作用而具有治疗AD的潜力。

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