Microbial diversity of inflamed and noninflamed gut biopsy tissues in inflammatory bowel disease

Authors

  • Shadi Sepehri MD,

    1. Department of Medical Microbiology and Infectious Diseases, Winnipeg, Manitoba, Canada
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  • Roman Kotlowski PhD,

    1. Department of Animal Science, Winnipeg, Manitoba, Canada
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  • Charles N. Bernstein MD,

    1. Department of Internal Medicine, Winnipeg, Manitoba, Canada
    2. University of Manitoba Inflammatory Bowel Disease Clinical and Research Centre, Winnipeg, Manitoba, Canada
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  • Denis O. Krause PhD

    Corresponding author
    1. Department of Medical Microbiology and Infectious Diseases, Winnipeg, Manitoba, Canada
    2. Department of Animal Science, Winnipeg, Manitoba, Canada
    3. University of Manitoba Inflammatory Bowel Disease Clinical and Research Centre, Winnipeg, Manitoba, Canada
    • Department of Animal Science, 236 Animal Science Building, University of Manitoba, Winnipeg R3T 2N2, Canada
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Abstract

Background: Inflammatory bowel disease (IBD) is a chronic gastrointestinal condition without any known cause or cure. An imbalance in normal gut biota has been identified as an important factor in the inflammatory process.

Methods: Fifty-eight biopsies from Crohn's disease (CD, n = 10), ulcerative colitis (UC, n = 15), and healthy controls (n = 16) were taken from a population-based case-control study. Automated ribosomal intergenic spacer analysis (ARISA) and terminal restriction fragment length polymorphisms (T-RFLP) were used as molecular tools to investigate the intestinal microbiota in these biopsies.

Results: ARISA and T-RFLP data did not allow a high level of clustering based on disease designation. However, if clustering was done based on the inflammation criteria, the majority of biopsies grouped either into inflamed or noninflamed groups. We conducted statistical analyses using incidence-based species richness and diversity as well as the similarity measures. These indices suggested that the noninflamed tissues form an intermediate population between controls and inflamed tissue for both CD and UC. Of particular interest was that species richness increased from control to noninflamed tissue, and then declined in fully inflamed tissue.

Conclusions: We hypothesize that there is a recruitment phase in which potentially pathogenic bacteria colonize tissue, and once the inflammation sets in, a decline in diversity occurs that may be a byproduct of the inflammatory process. Furthermore, we suspect that a better knowledge of the microbial species in the noninflamed tissue, thus before inflammation sets in, holds the clues to the microbial pathogenesis of IBD.

(Inflamm Bowel Dis 2007)

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