皮肤和肠道微生物群在银屑病(一种炎症性皮肤病)发病机制中的作用

Q2 Medicine
Daniel K. Hsu , Maxwell A. Fung , Hung-Lin Chen
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引用次数: 30

摘要

银屑病是一种慢性炎症性皮肤病,与表皮角化细胞增生和表皮免疫细胞过度活化有关。局部皮肤和肠道微生物组的组成与银屑病炎症和疾病严重程度的调节有关。由于不同的细菌可能会引起表皮免疫细胞和角质形成细胞的不同免疫或炎症反应,并且迄今为止没有单一病原体被强调为银屑病的原因,原始微生物生态系统中稳态的破坏(生态失调)可能会产生促进疾病的环境,并且作为一个整体可能是主要原因。一些研究已经提供证据表明,显性的IL-23/IL-17发病途径是由肠道和皮肤微生物群产生的代谢物调节的。本文综述了与银屑病临床表型发展相关的微生物组组成的功能表征的常用方法。微生物群调节免疫细胞和角质形成细胞的潜在机制也被提出。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of skin and gut microbiota in the pathogenesis of psoriasis, an inflammatory skin disease

Psoriasis is a chronic inflammatory skin disease associated with epidermal keratinocyte hyperplasia and epidermal immune cell over-activation. Compositions of both local skin and gut microbiome are linked to modulation of inflammation and disease severity in psoriasis. Owing to the situation that different bacteria may elicit differential immune or inflammatory responses from epidermal immune cells and keratinocytes, and to-date no single pathogen was highlighted to be responsible for psoriasis, disruption of homeostasis (dysbiosis) in the original microbial ecosystems may create a disease-promoting environment, and as a whole may be a primary causal factor. Several studies have provided evidence that the dominant IL-23/IL-17 pathogenesis pathway is regulated by metabolites produced by gut and skin microbiota. This review summarizes the approaches commonly used for functional characterization of the microbiome compositions associated with development of clinical phenotypes of psoriasis. The underlying mechanisms by which microbiota modulate immune cells and keratinocytes are also proposed.

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来源期刊
Medicine in Microecology
Medicine in Microecology Medicine-Gastroenterology
CiteScore
5.60
自引率
0.00%
发文量
16
审稿时长
76 days
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