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多糖可减轻二硝基氟苯诱导的类特应性皮炎小鼠的特应性皮炎症状并调节肠道微生物群。

polysaccharide reduce atopic dermatitis symptoms and modulate gut microbiota in DNFB-induced AD-like mice.

作者信息

Liang Yiheng, Liu Guangrong, Xie Lingna, Su Kewen, Chang Xia, Xu Yani, Chen Junsong, Zhu Zhenyuan, Yang Kaiye, Chen Huixiong, Du Zhiyun

机构信息

School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.

Guangdong Provincial Key Laboratory of Plant Resources Biorefinery, Guangdong University of Technology, Guangzhou, China.

出版信息

Front Physiol. 2022 Sep 9;13:976421. doi: 10.3389/fphys.2022.976421. eCollection 2022.

DOI:10.3389/fphys.2022.976421
PMID:36160845
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9500176/
Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease with a high prevalence worldwide. Increasing evidence suggests that the gut microbiota plays an important role in the pathogenesis of AD. In this study, we sought to verify the effect of polysaccharides (DCP) on AD induced by 2,4-Dinitrofluorobenzene (DNFB) in Balb/c mice regarding its impact on the intestinal microbiome. We found that 2-week oral administration of DCP improved AD-like symptoms and histological damage of skin, reduced mast cell infiltration, down-regulated the level of serum total IgE and the expression of pro-inflammatory cytokines such as TNF-α, IFN-γ, IL-4 and IL-6, and increased the expression level of anti-inflammatory cytokine IL-10. The beneficial effect of DCP was attributed to the restoration of the intestinal microbiome composition and the unbalance of the intestinal homeostasis. Our results indicated that DCP might be used as a promising novel microbiota-modulating agent for the treatment of AD.

摘要

特应性皮炎(AD)是一种在全球范围内患病率很高的慢性炎症性皮肤病。越来越多的证据表明,肠道微生物群在AD的发病机制中起重要作用。在本研究中,我们试图验证多糖(DCP)对2,4-二硝基氟苯(DNFB)诱导的Balb/c小鼠AD的影响,及其对肠道微生物组的作用。我们发现,连续2周口服DCP可改善AD样症状和皮肤组织学损伤,减少肥大细胞浸润,下调血清总IgE水平以及促炎细胞因子如TNF-α、IFN-γ、IL-4和IL-6的表达,并增加抗炎细胞因子IL-10的表达水平。DCP的有益作用归因于肠道微生物组组成的恢复和肠道稳态的失衡。我们的结果表明,DCP可能是一种有前景的新型微生物群调节剂,可用于治疗AD。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89a8/9500176/33063ee281a9/fphys-13-976421-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89a8/9500176/9b90cbadf629/fphys-13-976421-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89a8/9500176/91f274b90625/fphys-13-976421-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89a8/9500176/da5bcf8286ac/fphys-13-976421-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89a8/9500176/dda0873a554c/fphys-13-976421-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89a8/9500176/9c322dc213fb/fphys-13-976421-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89a8/9500176/33063ee281a9/fphys-13-976421-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89a8/9500176/9b90cbadf629/fphys-13-976421-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89a8/9500176/91f274b90625/fphys-13-976421-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89a8/9500176/da5bcf8286ac/fphys-13-976421-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89a8/9500176/dda0873a554c/fphys-13-976421-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89a8/9500176/9c322dc213fb/fphys-13-976421-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89a8/9500176/33063ee281a9/fphys-13-976421-g006.jpg

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