The intestine is continuously exposed to foreign materials including commensal bacteria. To maintain homeostasis, in addition to the physical and chemical barriers presented by epithelial cells, numerous kinds and numbers of immune cells exist in the intestines, which are affected by commensal bacteria, dietary materials, and their metabolites. Recent evidence has revealed the mechanism underlying the regulation of host immunity through the interaction between commensal bacteria and diets. Here, we describe the regulation of host immunity through commensal bacteria and diets.

T cells play a critical ro" in antigen-specific immune responses and their differentiation and function are affected by gut microbiota. αβ TCR expressing T cells are basically divided into CD4⁺ and CD8⁺ T cells. Among CD4⁺ T cells, T_H1 cells contribute to the c"arance of pathogen infections and their activation may cause development or exacerbation of autoimmune diseases. T_H2 cells serve as the main effector against helminth infection and also cause al"rgic reactions. CD8⁺ T cells play an important ro" in immunity against pathogens and cancers. In this review, we introduce intestinal bacteria that can affect the T_H1/ T_H2/CD8⁺ T cells-mediated immune response and diseases.

The gastrointestinal (GI) tract is recognized as the largest sensory organ in the body, as it is equipped with sophisticated mechanisms which constantly monitor the dynamic microenvironment within the tissues and lumen of the gut wall. The enteric nervous system (ENS) is the gut-intrinsic neural network which is composed of enteric neurons and glial cells and plays a central role in the sensing of gut environmental factors. ENS is thought to be involved in the regulation of virtually all aspects of GI functions, and its abnormalities can cause various chronic GI disorders, including irritable bowel syndrome (IBS). Since the ENS contains autonomously operating neural circuits, many of its functions are maintained without inputs from the brain. However, the ENS does serve as a relay station for the gut-brain axis. Current evidence suggests that the gut microbiota influences the development and functions of the ENS. However, the molecular mechanisms by which microbial factors regulate ENS physiology remain to be elucidated. Here, I review recent updates regarding microbial modifications of intestinal neural circuits.