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营养与特应性皮炎。

Nutrition and Atopic Dermatitis.

机构信息

Department of Dermatology, Nippon Medical School Chiba Hokusoh Hospital.

Department of Dermatology, Nippon Medical School.

出版信息

J Nippon Med Sch. 2021 Jun 30;88(3):171-177. doi: 10.1272/jnms.JNMS.2021_88-317. Epub 2021 Mar 9.

Abstract

Atopic dermatitis (AD) is a chronic eczematous disease characterized by T helper 2 (Th2) -shifted allergic immunity, skin barrier impairment, and pruritus. Oral intake of certain nutrients might help regulate AD. Serum 25-hydroxyvitamin D levels are often low in patients with AD, and oral vitamin D supplementation improves AD. Vitamin D increases regulatory T (Treg) cells, which promote tolerance to allergens and prevent allergic inflammation by inducing expression of filaggrin and cathelicidin in keratinocytes. Vitamin A strengthens Treg cells by inducing expression of forkhead box P3 and inhibits mediator release from mast cells and eosinophils. Serum levels of γ-linolenic acid and its metabolite, dihomo-γ-linolenic acid, are low in patients with AD, and oral γ-linolenic acid improves AD through anti-inflammatory prostaglandin D and E derived from dihomo-γ-linolenic acid. Eicosapentaenoic acid and docosahexaenoic acid ameliorate AD by suppressing production of leukotriene B, increasing ceramides in the stratum corneum, and through their metabolites, resolvin E1 and D1, which resolve inflammation. The probiotics Lactobacillus and Bifidobacteria improve the intestinal permeability barrier and induce Treg cells. Zinc levels in serum, hair, and erythrocytes are diminished in patients with AD. Zinc induces forkhead box P3 expression and increases Treg cells, and zinc-finger protein A20 suppresses nuclear factor-κB-dependent expression of inflammatory cytokines and cell-adhesion molecules. Oral supplementation of the above nutrients might have therapeutic or preventive roles in AD.

摘要

特应性皮炎(AD)是一种慢性湿疹性疾病,其特征为 T 辅助 2(Th2)型过敏免疫、皮肤屏障损伤和瘙痒。某些营养素的口服摄入可能有助于调节 AD。AD 患者的血清 25-羟维生素 D 水平通常较低,口服维生素 D 补充可改善 AD。维生素 D 可增加调节性 T(Treg)细胞,通过诱导角质形成细胞中丝聚蛋白和抗菌肽的表达,促进对过敏原的耐受并预防过敏炎症。维生素 A 通过诱导叉头框 P3 的表达来增强 Treg 细胞,并抑制肥大细胞和嗜酸性粒细胞释放介质。AD 患者的血清 γ-亚麻酸及其代谢物二同型-γ-亚麻酸水平较低,口服 γ-亚麻酸通过抗炎性前列腺素 D 和 E(来源于二同型-γ-亚麻酸)改善 AD。二十碳五烯酸和二十二碳六烯酸通过抑制白三烯 B 的产生、增加角质层中的神经酰胺以及通过其代谢物解析素 E1 和 D1 来缓解 AD,解析素 E1 和 D1 可解决炎症。益生菌乳杆菌和双歧杆菌可改善肠道通透性屏障并诱导 Treg 细胞。AD 患者的血清、头发和红细胞中的锌水平降低。锌诱导叉头框 P3 的表达并增加 Treg 细胞,锌指蛋白 A20 抑制核因子-κB 依赖性炎症细胞因子和细胞间黏附分子的表达。上述营养素的口服补充可能在 AD 中具有治疗或预防作用。

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