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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Ceramidase Activity in Bacterial Skin Flora as a Possible Cause of Ceramide Deficiency in Atopic Dermatitis
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Ceramidase Activity in Bacterial Skin Flora as a Possible Cause of Ceramide Deficiency in Atopic Dermatitis

机译：细菌性皮肤菌群中的神经酰胺酶活性可能是特应性皮炎中神经酰胺缺乏的可能原因

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摘要

A marked decrease in the content of ceramide has been reported in the horny layer of the epidermis in atopic dermatitis (AD). This decrease impairs the permeability barrier of the epidermis, resulting in the characteristic dry and easily antigen-permeable skin of AD, since ceramide serves as the major water-holding molecule in the extracellular space of the horny layer. On the other hand, the skin of such patients is frequently colonized by bacteria, most typically byStaphylococcus aureus, possessing genes such as those for sphingomyelinase, which are related to sphingolipid metabolism. We therefore tried to identify a possible correlation between the ceramide content and the bacterial flora obtained from the skin of 25 patients with AD versus that of 24 healthy subjects, using a thin-layer chromatographic assay of the sphingomyelin-associated enzyme activities secreted from the bacteria. The findings of the assay demonstrated that ceramidase, which breaks ceramide down into sphingosine and fatty acid, was secreted significantly more from the bacterial flora obtained from both the lesional and the nonlesional skin of patients with AD than from the skin of healthy subjects; sphingomyelinase, which breaks sphingomyelin down into ceramide and phosphorylcholine, was secreted from the bacterial flora obtained from all types of skin at similar levels for the patients with AD and the healthy controls. The finding that the skin of patients with AD is colonized by ceramidase-secreting bacteria thus suggests that microorganisms are related to the deficiency of ceramide in the horny layer of the epidermis, which increases the hypersensitivity of skin in AD patients by impairing the permeability barrier.
机译：据报告，特应性皮炎（AD）的表皮角质层中神经酰胺含量明显降低。由于神经酰胺在角质层细胞外空间中是主要的保水分子，因此这种减少削弱了表皮的通透性屏障，从而导致AD皮肤干燥且容易渗透抗原。另一方面，这类患者的皮肤经常被细菌定植，最常见的是被金黄色葡萄球菌所定植，细菌具有与鞘脂代谢相关的基因，如鞘磷脂酶基因。因此，我们试图通过薄层色谱分析细菌分泌的鞘磷脂相关酶的活性，来确定25例AD患者与24例健康受试者的皮肤中神经酰胺含量与细菌菌群之间的可能相关性。 。分析的结果表明，神经酰胺分解成神经鞘氨醇和脂肪酸的神经酰胺酶从患有AD的患者的病灶和非病灶皮肤获得的细菌菌群中分泌的比健康受试者的皮肤要多得多。鞘磷脂酶可将鞘磷脂分解为神经酰胺和磷酸胆碱，从AD患者和健康对照者从所有类型的皮肤获得的细菌菌群中以相似的水平分泌。因此，患有AD的患者的皮肤被分泌有神经酰胺酶的细菌所定殖的发现表明，微生物与表皮角质层中神经酰胺的缺乏有关，这通过损害渗透屏障而增加了AD患者的皮肤超敏性。

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