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논문 기본 정보

자료유형
학술저널
저자정보
Yunzhen Zhu (The First Afliated Hospital of Kunming Medical University) Juan Luo (The First Afliated Hospital of Kunming Medical University) Zhaoqing Yang (Kunming Medical University) Yinglei Miao (The First Afliated Hospital of Kunming Medical University)
저널정보
한국유전학회 Genes & Genomics Genes & Genomics Vol.42 No.10
발행연도
2020.1
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1,197 - 1,206 (10page)

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Background Previous investigations reported that the imbalance of intestinal microfora may be the initiation and promotion factor in the pathogenesis of infammatory bowel disease such as ulcerative colitis (UC). Glucocorticoid is a very important class of regulatory molecules in the body. The response of diferent individuals to glucocorticoids can be divided into glucocorticoid sensitive, glucocorticoid resistance and glucocorticoid dependence. Objective We aimed to investigate the diferences in intestinal microfora composition and related metabolic pathways in UC patients with these three diferent glucocorticoid response types. Methods The whole genomic DNA was extracted from fecal specimens. High-throughput sequencing technology was used to analyze the fecal 16S rRNA genome of UC patients with diferent glucocorticoid response types, and functional prediction was performed by PICRUSTs software. Results The results showed that the intestinal microfora of the three groups were mainly composed of Firmicutes, Proteobacteria and Bacteroidetes. Although the species abundance and diversity of intestinal microfora in UC patients difered little among the three groups, the composition of intestinal microfora showed signifcant heterogeneity, which directly led to diferences in the function of intestinal microbiota of UC patients with diferent glucocorticoid responses. Furthermore, of the 240 pathways, “PANTO-PWY: phosphopantothenate biosynthesis I”, “COA-PWY-1: coenzyme A biosynthesis II (mammalian)” and “PWY-4242: pantothenate and coenzyme A biosynthesis III” were signifcantly diferent in the three groups. Conclusions These results indicate that UC patients with diferent glucocorticoids response types have diferent bacterial compositions and functions, which lays a foundation for further study of glucocorticoid resistance in UC patients.

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