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P079 Association of gut microbiota with mucosal inflammation in ulcerative colitis

Quraishi M.N.*1,2, Rossiter A.3, Chung B.4,5, Beaumont M.6, Liaskou E.4, Horniblow R.1, Beggs A.1, Withers D.7, Ghosh S.2,8, Tselepis C.1, Hirschfield G.4, Iqbal T.H.1,2

1University of Birmingham, Institute of Cancer and Genomic Sciences, Birmingham, United Kingdom 2University Hospital Birmingham, Department of Gastroenterology, Birmingham, United Kingdom 3University of Birmingham, Institute of Microbiology and Infection, Birmingham, United Kingdom 4University of Birmingham, Centre for Liver Research and National Institute of Health Research (NIHR) Birmingham, Liver Biomedical Research Unit (BRU), Institute of Immunology and Immunotherapy, Birmingham, United Kingdom 5Oslo University Hospital Rikshospitalet, University of Oslo, Norwegian PSC Research Center and Institute of Clinical Medicine, Oslo, Norway 6Kings College London, Twin Research & Genetic Epidemiology, London, United Kingdom 7University of Birmingham, Institute of Immunology and Immunotherapy, Birmingham, United Kingdom 8University Hospital Birmingham, Institute of Translational Medicine, Birmingham, United Kingdom


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


We collected colonic biopsies from histologically confirmed areas of inflamed and non-inflamed colon from 15 patients with active left sided ulcerative colitis or proctosigmoiditis. DNA was extracted using the FASTSpin Kit and gut microbiota was characterized using 16s rRNA based analysis of the V3–V4 region (Illumina MiSeq). Quality control and operational taxonomic unit classification of sequences was executed using QIIME. As a marker of mucosal humoral immune responses, inflamed and non-inflamed colonic biopsy samples were cultured in media (RPMI + 10% FCS) for 1 to 3 days prior to measurement of immunoglobulin production (IgA, IgG and IgM) by ELISA.


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. Total immunoglobulin 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 regardless of inflammation.


We have demonstrated that the dysbiosis observed in patients with UC is consistent and is not influenced by mucosal inflammation or disease activity. Mucosal immunoglobulin production was not upregulated at sites of inflammation possibly suggestive of a uniform humoral response across the colon; although future work may uncover differences in antibody specificity to UC-associated dysbiosis. The mechanism for the complex interplay between the host immune system and gut microbiota in contributing to mucosal inflammation remains to be understood.