Recognition of, and interaction with, the gut microbiota August 12(Wed), 11:00 / Auditorium (1F), PBC Hiroshi Ohno RIKEN Center for Integrative Medical Sciences Our gut is colonized with a huge number of commensal gut microbiota: more than 100 trillions classified into 500~1,000 species. However, the gut does not unconditionally accept commensal microbiota. Our intestinal immune system somehow senses the kind and amount of bacteria existing in the gut lumen and tries to contain the total number and composition of the gut microbiota. M cells, a unique subset of intestinal epithelial cells, serve as a portal for luminal bacteria, with vigorous phagocytosis and transcytosis. M cells exist in the region of epithelium covering lymphoid follicles in the gut such as Peyer’s patch, and take up and transfer bacteria to the underneath dendritic cells to initiate mucosal immune responses. I would like to discuss molecular mechanisms for the differentiation and function of M cells. On the other hand, gut microbiota closely interact with the host and influence their physiology and pathology including host defense and immunity. However, the underlying mechanisms of how gut microbiota modulates host defense and immune system have poorly understood, since there has been no good way to solve the questions. To understand these mechanisms, we have proposed an integrated omics approach, where different levels of exhaustive analyses such as (meta) genomics, (meta)transcriptomics and metabolomics are combined. I would like to discuss our results obtained by applying this approach; mechanism of protecting mice from enterohemorrhagic Escherichia coli infectious death by bacterial acetate, and the induction of colonic regulatory T cell differentiation via epigenetic regulation by bacterial butyrate. Inquiry: AIM Administrative Team (Tel.279-8628, E-mail: varsha@ibs.re.kr)