Intestinal mucosal layers are colonized by a complex microbiota that provides beneficial effects under normal physiological conditions, but is capable of contributing to chronic inflammatory disease such as inflammatory bowel disease (IBD) in susceptible individuals. Studies have shown that the enteric microbiota may drive the development of the gut immune system and can induce immune homeostasis as well as contribute to the development of IBD although the precise etiology is still unknown. Therefore, intestinal microbes seem to play a key role in the disease pathogenesis. Especially, dysbiosis, which is a shift in the composition of enteric microbiota to a nonphysiologic composition, is associated with one or more defects in mucosal immune functions, including microbe recognition, barrier function, intercellular communication, and anti-microbial effector mechanisms. This review focuses on the impact of enteric microbiota on the development and perpetuation of IBD. In addition, interactions with enteric bacteria and mucosal cells, including intestinal epithelial cells, dendritic cells, and T cells, to induce immune responses at mucosal surfaces have been discussed in the point of IBD pathogenesis. Further extension of the knowledge of enteric microbiota may lead to insights on the pathogenesis and new therapeutic strategies for IBD.
Bacterial Physiological Phenomena ; Host-Pathogen Interactions ; Humans ; Inflammatory Bowel Diseases/*microbiology/pathology ; Intestinal Mucosa/immunology/microbiology ; Intestines/microbiology/pathology ; T-Lymphocytes/immunology/metabolism

Proliferative enteropathy was reproduced in IFN-gamma receptor knockout (IFN-gamma R-) mice by experimental infection with Lawsonia intracellularis (L. intracellularis). The cecum and the colon of the infected mice were evidently enlarged 2 weeks post infection. The presence of L. intracellularis was identified in the stool and the cecum of the mice after infection. However, high levels of IFN-gamma were detected in the sera of the infected mice 2 weeks PI. These data indicated that the IFN-gamma produced in the infected mice should have been utilized by it's receptor to elicit protective immune responses against L. intracellularis infections.
Animals ; DNA, Viral ; Desulfovibrionaceae Infections/*immunology/microbiology ; Interferon Type II/*immunology ; Intestinal Diseases/*immunology/microbiology ; Intestinal Mucosa/immunology ; Lawsonia Bacteria/*immunology/isolation&purification ; Mice ; Mice, Knockout ; Polymerase Chain Reaction ; Receptors, Interferon/physiology