The widely observed reduction in diversity of gut microbial ecology in inflammatory bowel disease [ 31, 32] may be a consequence of more specific functional changes.
Aberrant gut microbial composition, termed 'dysbiosis', has been reported in inflammatory bowel disease patients who are at increased risk for CRC development.
However, gut microbial modulation is not always initiated by medical intervention, and small bowel transplants used in cases of intestinal failure permit an opportunity for long-term study of the microbial ecology of the human small bowel.
However, alteration of the gut microbial composition is often linked to various pathological conditions, such as inflammatory bowel diseases, colon cancer and obesity.
Crohn's disease is an inflammatory bowel disease (IBD) with courses of recurrent inflammation, the etiology of which is likely rooted in the interplay of gut microbial imbalances (dysbiosis) and host immunity [ 1].
This review focuses on the microbial ecology of the gut in inflammatory bowel diseases and on how recent studies provide an impetus for using carefully designed, comparative metagenomic approaches to delve into the structure and activities of the gut microbial community and its interrelationship with the immune system.
These observations may contribute to creation of a cytotoxic environment in the bowel, [ 42] also leading to shifts in the gut microbial-host metabolic crosstalk as demonstrated by faecal, urinary, and host metabolomic profiles [ 23, 42, 43].
We are host to a hundred trillion or so bacteria, and every portion of the bowel represents a different microbial ecosystem.
"Throughout early life, the immune system takes maturational cues from the environment in the form of microbial stimulation, bowel flora, mother's milk, and dietary factors.
It is characterised by abnormal villous and crypt architecture, heightened T cell-mediated inflammation and increased epithelial permeability secondary to impaired tight junction function [ 2, 3] which results in reduced small bowel absorptive capacity, increased microbial translocation and systemic inflammation [ 4].
