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首页> 外文期刊>Allergy >Decreased serum LL-37 and vitamin D3 levels in atopic dermatitis: Relationship between IL-31 and oncostatin M
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Decreased serum LL-37 and vitamin D3 levels in atopic dermatitis: Relationship between IL-31 and oncostatin M

机译：特应性皮炎血清LL-37和维生素D3水平降低：IL-31与制瘤素M的关系

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Background Skin lesions with atopic dermatitis (AD) are associated with dysregulated expression of LL-37 and enhanced expression of IL-22, thymic stromal lymphopoietin (TSLP), IL-25, IL-31, and oncostatin M. Vitamin D3 enhances LL-37 production in keratinocytes. This study aimed to examine the serum levels of LL-37 and vitamin D3 and their regulation of cytokine production in patients with AD. Methods Serum levels of LL-37 and 25-hydroxyvitamin D3 were analyzed by ELISA. The effects of 1,25-dihydroxyvitamin D3 or LL-37 on cytokine production in T cells or keratinocytes were analyzed by ELISA and real-time PCR. Results Serum levels of LL-37 and 25-hydroxyvitamin D3 were decreased in patients with AD compared to normal donors and were correlated in both groups. Serum levels of LL-37 correlated with those of oncostatin M and IL-31 in normal donors and patients with AD, while 25-hydroxyvitamin D3 levels did so only in normal donors. 1,25-dihydroxyvitamin D3 increased LL-37 production in human keratinocytes and neutrophils. 1,25-dihydroxyvitamin D3 and LL-37 enhanced the oncostatin M and IL-31 production in CD3/28-stimulated T cells, but did not alter IL-25 and TSLP production in TNF-α-stimulated keratinocytes. In CD3/28-stimulated T cells, 1,25-dihydroxyvitamin D3 reduced the IL-22 production, while LL-37 enhanced it. These effects of 1,25-dihydroxyvitamin D3 and LL-37 were suppressed by vitamin D receptor antagonist and pertussis toxin, respectively. Conclusions Systemic vitamin D3 levels are reduced in patients with AD, which may contribute to decreased systemic LL-37 levels. LL-37 may systemically potentiate the oncostatin M and IL-31 production in normal donors and patients with AD, while vitamin D3 may do so only in normal donors.
机译：背景特应性皮炎（AD）的皮肤病变与LL-37的表达失调和IL-22，胸腺基质淋巴细胞生成素（TSLP），IL-25，IL-31和抑瘤素M的表达增强有关。维生素D3增强LL-37在角质形成细胞中产生37种。本研究旨在检查AD患者的LL-37和维生素D3的血清水平及其对细胞因子产生的调节。方法采用ELISA法检测血清LL-37和25-羟维生素D3水平。通过ELISA和实时PCR分析了1，25-二羟基维生素D3或LL-37对T细胞或角质形成细胞中细胞因子产生的影响。结果AD患者的血清LL-37和25-羟基维生素D3的水平较正常供体下降，并且两组之间相关。正常供体和AD患者的血清LL-37水平与抑癌素M和IL-31水平相关，而25-羟维生素D3水平仅在正常供体中相关。 1,25-二羟基维生素D3增加了人类角质形成细胞和嗜中性粒细胞中LL-37的产生。 1,25-二羟基维生素D3和LL-37增强了CD3 / 28刺激的T细胞中制瘤素M和IL-31的产生，但不改变TNF-α刺激的角质形成细胞中IL-25和TSLP的产生。在CD3 / 28刺激的T细胞中，1,25-二羟基维生素D3降低了IL-22的产生，而LL-37增强了它。 1,25-二羟基维生素D3和LL-37的这些作用分别被维生素D受体拮抗剂和百日咳毒素抑制。结论AD患者体内维生素D3水平降低，这可能导致全身LL-37水平降低。 LL-37可以在正常供体和AD患者中全身增强制瘤素M和IL-31的生成，而维生素D3仅在正常供体中可以增强。

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