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特应性皮炎的上皮屏障功能障碍:一个连接微生物组改变和免疫失调的皮肤-肠道-肺模型。

Epithelial barrier dysfunctions in atopic dermatitis: a skin-gut-lung model linking microbiome alteration and immune dysregulation.

机构信息

University of Southern California Keck School of Medicine, Los Angeles, CA, U.S.A.

The Warren Alpert Medical School, Brown University, Providence, RI, U.S.A.

出版信息

Br J Dermatol. 2018 Sep;179(3):570-581. doi: 10.1111/bjd.16734. Epub 2018 Jul 11.

DOI:10.1111/bjd.16734
PMID:29761483
Abstract

BACKGROUND

Atopic dermatitis is a systemic disorder characterized by abnormal barrier function across multiple organ sites. Causes of epidermal barrier breakdown are complex and driven by a combination of structural, genetic, environmental and immunological factors. In addition, alteration in microflora diversity can influence disease severity, duration, and response to treatment. Clinically, atopic dermatitis can progress from skin disease to food allergy, allergic rhinitis, and later asthma, a phenomenon commonly known as the atopic march. The mechanism by which atopic dermatitis progresses towards gastrointestinal or airway disease remains to be elucidated.

OBJECTIVES

This review addresses how epithelial dysfunction linking microbiome alteration and immune dysregulation can predispose to the development of the atopic march.

METHODS

A literature search was conducted using the PubMed database for relevant articles with the keywords 'atopic dermatitis', 'epithelial barrier', 'skin', 'gut', 'lung', 'microbiome' and 'immune dysregulation'.

RESULTS

Initial disruption in the skin epidermal barrier permits allergen sensitization and colonization by pathogens. This induces a T helper 2 inflammatory response and a thymic stromal lymphopoietin-mediated pathway that further promotes barrier breakdown at distant sites, including the intestinal and respiratory tract.

CONCLUSIONS

As there are no immediate cures for food allergy or asthma, early intervention aimed at protecting the skin barrier and effective control of local and systemic inflammation may improve long-term outcomes and reduce allergen sensitization in the airway and gut.

摘要

背景

特应性皮炎是一种全身性疾病,其特征是多个器官部位的表皮屏障功能异常。表皮屏障破坏的原因复杂,由结构、遗传、环境和免疫因素共同驱动。此外,微生物群落多样性的改变会影响疾病的严重程度、持续时间和治疗反应。临床上,特应性皮炎可从皮肤疾病进展为食物过敏、过敏性鼻炎,进而发展为哮喘,这一现象通常被称为特应性进行曲。特应性皮炎向胃肠道或气道疾病进展的机制仍有待阐明。

目的

本综述探讨了上皮功能障碍如何通过微生物群改变和免疫失调导致特应性进行曲的发生。

方法

使用 PubMed 数据库进行文献检索,关键词为“特应性皮炎”、“上皮屏障”、“皮肤”、“肠道”、“肺部”、“微生物群”和“免疫失调”。

结果

皮肤表皮屏障的初始破坏允许过敏原致敏和病原体定植。这会诱导辅助性 T 细胞 2 型炎症反应和胸腺基质淋巴细胞生成素介导的途径,进一步促进远处部位(包括肠道和呼吸道)的屏障破坏。

结论

由于目前尚无针对食物过敏或哮喘的即时治愈方法,早期干预旨在保护皮肤屏障并有效控制局部和全身炎症,可能会改善长期结局并减少气道和肠道中的过敏原致敏。

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