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The gut microbiota is a complex community that consists of 10-10 organisms per gram of colonic contents and over 150-fold more genes than the human genome. This community has evolved with its eukaryotic host to form a mutualistic relationship. It has been known that the microbiota is involved in the production of vitamins, the breakdown of dietary substances and the maturation of the immune system. Recent work has expanded the role of the microbiota in human health. The microbiota has been implicated in the regulation of fat storage and diseases such as ulcers, diabetes, obesity, cardiovascular disease, and inflammatory bowel disease (IBD). The work in this dissertation focuses on the role of the microbiota in IBD, a disease of unknown etiology. Several factors contribute to the development of disease, including environmental factors, host genetics, the immune response, and the gut microbiota. An environmental factor that has become increasingly recognized as a critical component in shaping the microbiota is the use of antibiotics and the potential link to IBD. The research summarized in chapter 2 reveals the effects that antibiotics have on a limited microbiota, the altered Schaedler flora (ASF). Use of a limited microbiota affords the ability to monitor effects of antibiotics on the entire community that would be missed when using a conventional microbiota. Following treatment with ampicillin, mice harboring the ASF developed more severe disease in response to a colitic insult than did mice bearing a conventional microbiota, indicating a central role for the microbiota in reducing disease severity. Those conventional mice that received ampicillin prior to colitic insult revealed that the ASF

Impact of antibiotic use, alternative therapies and inflammation on the intestinal microbiota