Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, China.
Graduate School, Capital Medical University, Beijing, China.
Front Cell Infect Microbiol. 2021 Apr 1;11:605825. doi: 10.3389/fcimb.2021.605825. eCollection 2021.
BACKGROUND: Increasing evidence has shown that alterations in the intestinal microbiota play an important role in the pathogenesis of psoriasis. The existing relevant studies focus on 16S rRNA gene sequencing, but in-depth research on gene functions and comprehensive identification of microbiota is lacking. OBJECTIVES: To comprehensively identify characteristic gut microbial compositions, genetic functions and relative metabolites of patients with psoriasis and to reveal the potential pathogenesis of psoriasis. METHODS: DNA was extracted from the faecal microbiota of 30 psoriatic patients and 15 healthy subjects, and metagenomics sequencing and bioinformatic analyses were performed. The Kyoto Encyclopedia of Genes and Genomes (KEGG) database, cluster of orthologous groups (COG) annotations, and metabolic analyses were used to indicate relative target genes and pathways to reveal the pathogenesis of psoriasis. RESULTS: Compared with healthy individuals, the gut microbiota of psoriasis patients displayed an alteration in microbial taxa distribution, but no significant difference in microbial diversity. A distinct gut microbial composition in patients with psoriasis was observed, with an increased abundance of the phyla , and and genera , , and and a decreased abundance of the phyla and and genera , and . A total of 134 COGs were predicted with functional analysis, and 15 KEGG pathways, including lipopolysaccharide (LPS) biosynthesis, WNT signaling, apoptosis, bacterial secretion system, and phosphotransferase system, were significantly enriched in psoriasis patients. Five metabolites, hydrogen sulfide (HS), isovalerate, isobutyrate, hyaluronan and hemicellulose, were significantly dysregulated in the psoriatic cohort. The dysbiosis of gut microbiota, enriched pathways and dysregulated metabolites are relevant to immune and inflammatory response, apoptosis, the vascular endothelial growth factor (VEGF) signaling pathway, gut-brain axis and brain-skin axis that play important roles in the pathogenesis of psoriasis. CONCLUSIONS: A clear dysbiosis was displayed in the gut microbiota profile, genetic functions and relative metabolites of psoriasis patients. This study is beneficial for further understanding the inflammatory pathogenesis of psoriasis and could be used to develop microbiome-based predictions and therapeutic approaches.
背景:越来越多的证据表明,肠道微生物群的改变在银屑病的发病机制中起着重要作用。现有相关研究主要集中在 16S rRNA 基因测序上,但对基因功能的深入研究和微生物群的综合鉴定还很缺乏。
目的:全面鉴定银屑病患者的特征肠道微生物组成、遗传功能和相关代谢物,揭示银屑病的潜在发病机制。
方法:从 30 名银屑病患者和 15 名健康对照者的粪便微生物中提取 DNA,进行宏基因组测序和生物信息学分析。使用京都基因与基因组百科全书(KEGG)数据库、直系同源群(COG)注释和代谢分析来指示相对靶基因和途径,以揭示银屑病的发病机制。
结果:与健康个体相比,银屑病患者的肠道微生物群显示出微生物分类群分布的改变,但微生物多样性没有显著差异。观察到银屑病患者的肠道微生物组成明显不同,厚壁菌门、拟杆菌门和变形菌门的丰度增加,放线菌门和梭杆菌门的丰度减少,而 、 、 、 、 和 等属的丰度增加, 、 和 等属的丰度减少。通过功能分析预测了 134 个 COG,银屑病患者中显著富集了 15 个 KEGG 途径,包括脂多糖(LPS)生物合成、WNT 信号、细胞凋亡、细菌分泌系统和磷酸转移酶系统。在银屑病队列中,有 5 种代谢物(硫化氢(HS)、异戊酸、异丁酸、透明质酸和半纤维素)明显失调。肠道微生物群的失调、富集途径和失调代谢物与免疫和炎症反应、细胞凋亡、血管内皮生长因子(VEGF)信号通路、肠-脑轴和脑-皮轴有关,这些在银屑病的发病机制中起着重要作用。
结论:银屑病患者的肠道微生物群谱、遗传功能和相关代谢物明显失调。本研究有助于进一步了解银屑病的炎症发病机制,并可用于开发基于微生物组的预测和治疗方法。
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