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PTH-102 Association of gut microbiota with mucosal inflammation in ulcerative colitis
  1. MN Quraishi1,
  2. A Rossiter2,
  3. B Chung3,
  4. M Beaumont4,
  5. E Liaskou3,
  6. R Horniblow1,
  7. A Beggs1,
  8. D Withers5,
  9. S Ghosh6,
  10. C Tselepis1,
  11. G Hirschfield3,
  12. T Iqbal1
  1. 1Institute of Cancer and Genomic Sciences
  2. 2Institute of Microbiology and Infection
  3. 3Centre for Liver Research, Liver Biomedical Research Unit, University of Birmingham, Birmingham
  4. 4Twin Research and Genetic Epidemiology, Kings College London, London
  5. 5Institute of Immunology and Immunotherapy
  6. 6Institute of Translational Medicine, University of Birmingham, Birmingham, UK


Introduction Disturbance in gut microbiota (dysbiosis) is a characteristic feature of ulcerative colitis (UC). It remains unclear whether this dysbiosis contributes to disease pathogenesis by driving immune dysregulation or is merely secondary to mucosal inflammation. We aimed to determine whether dysbiosis varied between areas of inflamed and non-inflamed colon in patients with UC and whether this was associated with a humoral immune response.

Method We collected colonic biopsies from histologically confirmed areas of inflamed and non-inflamed colon from 15 patients with active UC. DNA was extracted and gut microbiota was characterised using 16s rRNA based analysis. Inferred metagenomic analysis for microbial function was performed by PICRUSt. As a marker of mucosal humoral immune responses, inflamed and non-inflamed colonic biopsy samples were cultured for 1 to 3 days prior to measurement of total immunoglobulin (Ig) production by ELISA.

Results Consistent with previous observations patients with UC demonstrated reduced bacterial diversity with an increase in Proteobacteria, Bacteroides and Clostridiales species along with a decrease in Firmicutes to Bacteroides ratio. No differences were found in the microbial diversity nor phylae and genera in mucosally adherent gut microbiota between inflamed and non-inflamed colonic segments in patients with active UC. This observation was also seen when patients were subdivided based on disease activity as defined by Mayo scoring. PICRUSt analysis revealed genes associated with bacterial chemotaxis, motility and flagellar assembly were enriched in the inflamed tissue. Total Ig production did not differ between inflamed (n=6, mean 4966 +/- sd 3670 ng/ml) and non-inflamed tissue (n=11; mean 5756 +/- sd 8989 ng/ml; p>0.05) suggesting that equal numbers of antibody-producing B cells are present.

Conclusion We have demonstrated that the dysbiosis observed in patients with UC is consistent and is not influenced by mucosal inflammation or disease activity. Genes associated with bacterial invasion and flagellin are enriched at sites of inflammation. Mucosal Ig production was not upregulated at sites of inflammation possibly suggestive of a uniform humoral response. These functional pathways in colitis associated inflammation provide insight into contribution of microbiota in its pathogenesis.

Disclosure of Interest None Declared

  • Microbiome
  • Ulcerative colitis

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