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Intestinal Microbiology and Ecology in Inflammatory Bowel Disease

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Crohn's Disease and Ulcerative Colitis

Abstract

The human gastrointestinal tract contains a rich and abundant collection of microbes, which is collectively termed the microbiota. Colonization of the human body by microbes appears to occur in a reasonably reproducible manner and the adult microbiota is predominantly composed of just four bacterial phyla. However, within these phyla there are thousands of individual species and strains that are capable of colonizing the human intestinal tract. This complexity is further complicated by the fact that there appears to be only limited overlap in species composition between individuals. Furthermore, within individuals it appears that there are also temporal and spatial fluctuations in species abundance.

During the long co-evolution of humans and their microbiota a mutualistic relationship has developed and under normal circumstances the microbiota is considered to play a number of key roles in the maintenance of host health. However, it is also the source of numerous antigens, meaning that a constant balance must be maintained between the host’s immune system and the microbiota. If this balance breaks down inflammation may result and a number of lines of evidence implicate the intestinal microbiota in the development and progression of inflammatory bowel disease. Indeed there is now increasing evidence that there are distinctive differences in overall microbiota structure, such as reduced bacterial diversity and reduced temporal stability, in individuals with IBD compared to healthy individuals. However, detecting a direct causal link has proved to be more difficult and, at present, there is no conclusive evidence that particular species or distinctive overall microbiota compositions lead to IBD development.

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Correspondence to Alan W. Walker BSc (Hons), PhD .

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Walker, A.W. (2012). Intestinal Microbiology and Ecology in Inflammatory Bowel Disease. In: Baumgart, D. (eds) Crohn's Disease and Ulcerative Colitis. Springer, Boston, MA. https://doi.org/10.1007/978-1-4614-0998-4_5

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