Abstract ED06-02: Understanding the structure and function of the gut microbiota

Abstract

Abstract Until recently, the study of complex microbial communities was limited by the culture-based methodologies that only captured a subset of the diversity present. The advent of molecular methods for the study of microbial consortia has allowed us to greatly increase our understanding of the structure, function and dynamics of the indigenous human microbiota. In this opening lecture of the session I will introduce the techniques and strategies for studying the structure and function of complex consortia of microbes, with a focus on the community that inhabits the gastrointestinal tract. Using the example of Clostridium difficile infection following antibiotic administration as an example, I will demonstrate how changes in the community structure of the gut microbiota can be monitored over time. The associated functional changes associated with changes in microbial community structure will be discussed. We have recently applied culture-independent molecular methods, largely based on retrieval of 16S rRNA-encoding gene sequences, to investigate the role of the indigenous microbiota in C. difficile infection (CDI). Through studies of human patients with CDI we have demonstrated that recurrent disease is associated with an overall decrease in the diversity of the fecal microbiota. We have leveraged a recently described murine model of CDI to conduct more detailed studies of the role of the microbiota in C. difficile infection. Data from this model system indicates that a subset of the indigenous microbiota is important in mediating colonization resistance against C. difficile and possibly in modulating the effects of C. difficile toxin. This example will allow the audience to understand and appreciate the growing number of studies that are examining associations between the community structure of the gut microbiota and a variety of disease states including colorectal cancer. Citation Information: Cancer Prev Res 2010;3(12 Suppl):ED06-02.