The gut metagenomics and metabolomics signature in patients with inflammatory bowel disease

被引:0
作者
Xinwei Xu
Dickson Kofi Wiredu Ocansey
Sanhua Hang
Bo Wang
Samuel Amoah
Chengxue Yi
Xu Zhang
Lianqin Liu
Fei Mao
机构
[1] Jiangsu University,Key Laboratory of Medical Science and Laboratory Medicine of Jiangsu Province, School of Medicine
[2] Affiliated Danyang Hospital of Nantong University,The People’s Hospital of Danyang
[3] Huai’an Maternity and Children Hospital,Directorate of University Health Services
[4] University of Cape Coast,School of Medical Technology
[5] PMB,undefined
[6] Zhenjiang College,undefined
来源
Gut Pathogens | / 14卷
关键词
Inflammatory bowel disease; Metabolomics; Metagenomics; Gut bacteria; Differential metabolites;
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学科分类号
摘要
Inflammatory bowel disease (IBD), a chronic gut immune dysregulation and dysbiosis condition is rapidly increasing in global incidence. Regardless, there is a lack of ideal diagnostic markers, while conventional treatment provides scarce desired results, thus, the exploration for better options. Changes in the gut microbial composition and metabolites either lead to or are caused by the immune dysregulation that characterizes IBD. This study examined the fecal metagenomics and metabolomic changes in IBD patients. A total of 30 fecal samples were collected from 15 IBD patients and 15 healthy controls for 16S rDNA gene sequencing and UHPLC/Q-TOF-MS detection of metabolomics. Results showed that there was a severe perturbation of gut bacteria community composition, diversity, metabolites, and associated functions and metabolic pathways in IBD. This included a significantly decreased abundance of Bacteroidetes and Firmicutes, increased disease-associated phyla such as Proteobacteria and Actinobacteria, and increased Escherichiacoli and Klebsiellapneumoniae in IBD. A total of 3146 metabolites were detected out of which 135 were differentially expressed between IBD and controls. Metabolites with high sensitivity and specificity in differentiating IBD from healthy individuals included 6,7,4′-trihydroxyisoflavone and thyroxine 4′-o-.beta.-d-glucuronide (AUC = 0.92), normorphine and salvinorin a (AUC = 0.90), and trichostachine (AUC = 0.91). Moreover, the IBD group had significantly affected pathways including primary bile acid biosynthesis, vitamin digestion and absorption, and carbohydrate metabolism. This study reveals that the combined evaluation of metabolites and fecal microbiome can be useful to discriminate between healthy subjects and IBD patients and consequently serve as therapeutic and diagnostic targets.
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