BMC Gastroenterology (Jan 2019)

Role of colonic microbiota in the pathogenesis of ulcerative colitis

  • Ling-yan Pei,
  • Yu-shi Ke,
  • Huan-hu Zhao,
  • Lin Wang,
  • Chao Jia,
  • Wei-zhi Liu,
  • Qian-hui Fu,
  • Meng-ni Shi,
  • Jian Cui,
  • Shu-chun Li

DOI
https://doi.org/10.1186/s12876-019-0930-3
Journal volume & issue
Vol. 19, no. 1
pp. 1 – 11

Abstract

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Abstract Background Recent studies have found gut microbiota to be closely associated with onset and perpetuation of UC. Currently, studies about gut microbiota have mainly covered samples collected from the intestinal lumen. However, the luminal flora is only part of the gut microbiota. Studies of the changes in mucosal flora under pathological conditions have been lacking. In this study, we investigated the correlation between the onset of UC and flora changes in different intestinal layers. Methods The dextran sulfate sodium(DSS)-induced UC model was established by exposing mice to cycles of DSS. The luminal contents, an inner mucus layer, and outer mucus layer were harvested under sterile conditions. The samples were then analyzed using high-throughput sequencing of 16S rRNA V3 + V4 amplicons. The colonic microbiota composition and diversity were analyzed and compared using MetaStat, LefSe, multivariate analysis of variance, and spatial statistics. Results The DSS-induced UC mouse model was successfully established. The diversity of the microbiota from luminal content, the outer mucus layer, and inner mucus layer were significantly different in both control and UC model groups. The statistically different OTUs belonged to Lachnospiraceae and Ruminococcaceae families within the order Clostridiales were mainly localized to the outer mucus layer. Conclusions The alterations in flora composition and diversity mainly occurred in the colonic outer mucus layer. The change of flora in the colonic mucus layers is of great significance in the understanding of common features of gut flora in IBD and the understanding of the relationship between gut flora and disease progression.

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