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

Animals ; Anti-Bacterial Agents ; administration & dosage ; Escherichia coli ; Female ; Galactosylceramides ; immunology ; Gastric Mucosa ; pathology ; Gastritis, Atrophic ; pathology ; Helicobacter Infections ; complications ; drug therapy ; Helicobacter pylori ; pathogenicity ; Humans ; Inflammation ; pathology ; Intestines ; microbiology ; Levofloxacin ; Lymphocyte Activation ; Male ; Natural Killer T-Cells ; microbiology ; Ofloxacin ; administration & dosage ; Sphingomonas ; Stomach ; pathology

Verocytotoxic Escherichia (E.) coli strains are responsible for swine oedema disease, which is an enterotoxaemia that causes economic losses in the pig industry. The production of a vaccine for oral administration in transgenic seeds could be an efficient system to stimulate local immunity. This study was conducted to transform tobacco plants for the seed-specific expression of antigenic proteins from a porcine verocytotoxic E. coli strain. Parameters related to an immunological response and possible adverse effects on the oral administration of obtained tobacco seeds were evaluated in a mouse model. Tobacco was transformed via Agrobacteium tumefaciens with chimeric constructs containing structural parts of the major subunit FedA of the F18 adhesive fimbriae and VT2e B-subunit genes under control of a seed specific GLOB promoter. We showed that the foreign Vt2e-B and F18 genes were stably accumulated in storage tissue by the immunostaining method. In addition, Balb-C mice receiving transgenic tobacco seeds via the oral route showed a significant increase in IgA-positive plasma cell presence in tunica propria when compared to the control group with no observed adverse effects. Our findings encourage future studies focusing on swine for evaluation of the protective effects of transformed tobacco seeds against E. coli infection.
Administration, Oral ; Agrobacterium tumefaciens ; Animals ; Antigens, Bacterial/genetics/metabolism ; Bacterial Vaccines/administration & dosage/adverse effects/*pharmacology ; Edema Disease of Swine/*immunology/microbiology ; Escherichia coli Infections/immunology/microbiology/*veterinary ; Escherichia coli Proteins/*genetics/metabolism ; Female ; Fimbriae Proteins/genetics/metabolism ; Genetic Engineering ; Intestines/immunology/microbiology/pathology ; Mice ; Mice, Inbred BALB C ; Models, Animal ; Plants, Genetically Modified/*genetics/metabolism ; Seeds/genetics/metabolism ; Shiga Toxin 2/genetics/metabolism ; Shiga-Toxigenic Escherichia coli/genetics/immunology/*pathogenicity ; Swine ; Tobacco/*genetics/metabolism ; Virulence Factors/genetics/metabolism