2015 年 35 巻 1 号 p. 028-041
The mammalian gastrointestinal tract, the site of nutrient digestion and absorption, harbors a dense microbial community. The intestinal immune system can distinguish between symbiotic bacteria and pathogens, and activates pro-inflammatory responses against pathogenic bacteria for host defense while remaining unresponsive to the beneficial microbes and dietary antigens. Abnormal activity of innate immunity, which directs the development of adaptive immunity, causes the onset and/or progression of several inflammatory diseases. Thus, activity of innate immunity is finely regulated in the gut. Inflammatory bowel disease is a chronic inflammatory disorder caused by alteration of several factors, such as host genetics, commensal bacteria and diet-derived compounds and metabolites. In intestinal mucosa, multiple innate immune cells have been identified and some populations play a crucial role in the maintenance of gut homeostasis by preventing inadequate adaptive immune responses while others are implicated in the pathogenesis of inflammatory bowel disease by driving Th1 and Th17 responses. In addition, recent studies demonstrated that dietary components and their metabolites produced by commensal bacteria contribute to the generation of a unique intestinal environment and further regulation of a variety of immune responses. Accordingly, alterations of intestinal microbial composition and perturbation of metabolites can trigger intestinal inflammation by inducing inadequate innate/adaptive immune responses.