| Summary: | This thesis has addressed both the possibility of a potential pathogenic organism, or a shift in the mucosal microbial community, associated with UC. Firstly by developing a dual molecular technique to detect <i>Helicobacteraceae </i>species in colonoscopic biopsies from the human colon alongside attempting to culture these organisms and secondly by assessing the mucosal colonic microbiota in both detail by the construction of phylogenetic clone libraries and broadly by comparison of DGGE profiles between inflamed and uninvolved mucosa during active disease. The dual molecular approach demonstrated that enterohepatic <i>Helicobacter </i>prevalence was significantly higher in the UC cohort compared to controls (30 of 77 versus 2 of 59, p<0.0001). These findings suggest that these species, for which there is significant evidence from animal models for initiation of colonic inflammation, warrant consideration as potential pathogenic entities in UC. Detailed assessment of the colonic mucosal microbial community by the construction of clone libraries in this thesis revealed a wide variation in the constituents of the microbiota between individuals making comparisons between groups difficult with the small numbers of subjects. Comparison of DGGE profiles between inflamed and uninvolved mucosa indicated differences in only 12 of the 36 subjects. Analysis to identify factors associated with this showed a statistically significantly relationship with no bowel preparation prior to the colonoscopy, 5ASA therapy, and antibiotic treatment but not with mucosal state or extent of disease, suggesting that it is not the inflammation itself that results in the microbial shifts seen between the inflamed and uninvolved mucosa in active UC.
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