Pharyngeal Microbiome in Atopic Dermatitis: A 16S rRNA Sequencing Study

生物 发病机制 微生物群 普雷沃菌属 拟杆菌 微生物学 特应性皮炎 梭杆菌 肠道菌群 梭杆菌门 免疫学 厚壁菌 16S核糖体RNA 遗传学 细菌
作者
Tian Zhang,Jianxin Shi,Xinxin Li,Huan Liu,Yuegang Wei,Hongmin Li
出处
期刊:Experimental Dermatology [Wiley]
卷期号:34 (1)
标识
DOI:10.1111/exd.70031
摘要

ABSTRACT While recent studies have demonstrated the involvement of the skin and gut microbiome in the pathogenesis of atopic dermatitis (AD), the influence of pharyngeal microbiota on AD remains unclear. This study aims to explore disparities in the composition of pharyngeal flora among AD patients and their potential role in the pathogenesis of AD. Between March and May 2023, 30 patients with AD at the outpatient department of Jiangsu Provincial Traditional Chinese Medicine Hospital were recruited, along with 20 healthy subjects, underwent 16S rRNA sequencing on pharyngeal swabs. Pharyngeal taxonomic biomarkers of AD were identified using linear discriminant analysis effect size (LEfSe), and phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt2) was employed to predict potential functional metabolic pathways of bacteria with differential abundance. Significant variations were observed in the microbiota composition between the two study groups. The Pharynx of AD patients exhibited a notably higher relative abundance of Granulicatella , Pseudomonas , and Acinetobacter compared to healthy volunteers. Conversely, the relative abundance of Prevotella , Porphyromonas , Campylobacter , Lactobacillaceae , Treponema , Megasphaera , Selenomonas , and Oribacterium was lower in AD patients. According to the metabolic functional enrichment annotations predicted by PICRUSt2, bacteria with differential abundance may be involved in the pathogenesis of AD through two metabolic pathways, namely chondroitin sulfate degradation and chitin derivatives degradation. AD patients displayed distinctive microbiota profiles compared to healthy controls. These findings imply a pivotal role of pharyngeal microbiota in the pathogenesis of AD, offering novel perspectives for AD treatment strategies.
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