title: Inflammatory bowel disease: dysfunction of GALT and gut bacterial flora (II).
abstract: The precise cause(s) of Crohn's disease and ulcerative colitis are unknown. From animal models and human studies it is well established that gut bacterial flora are essential for inducing the bowel inflammation. Animal models, when kept in a germ-free environment, do not develop colitis until the gut flora is reconstituted. It is not clear whether the bacterial antigens (Ags) from the normal flora or some other pathogenic bacterial Ags induce/propagate the inflammatory process in inflammatory bowel disease (IBD). Despite extensive research it has not been possible to identify any specific bacteria or virus as a credible cause of IBD. Recent understanding of quorum sensing molecules (QSMs) secreted by bacteria helps to explain the community behaviour in bacterial species. When QSMs reach a defined concentration, they activate bacterial proliferation and a number of virulence genes. Also, these molecules have been found to modulate the immune system to the advantage of the gut bacteria. They have not been well studied, however, in the gut. Inappropriate secretion of QSMs may alter the gut-associated lymphoid tissue (GALT) and, thereby, deregulate the immune tolerance normally present. Usefulness of probiotics and their immune modulating effects are being increasingly reported. Probiotics are also being used in the treatment of IBD. The interaction between the epithelial cells and the gut flora is very important as this is the first line of contact; this interaction may determine the induction of tolerance and mucosal integrity or immune activity, tissue inflammation and abnormal permeability. The latter is documented in patients with IBD and their healthy relatives. This may be an important factor in disruption of mucosal integrity and GALT dysfunction.
authors.affiliation: Department of Surgery, Queens Medical Centre, University of Nottingham, Nottingham.
authors.forename: P
authors.initials: P
authors.lastname: Chandran
authors.forename: S
authors.initials: S
authors.lastname: Satthaporn
authors.forename: A
authors.initials: A
authors.lastname: Robins
authors.forename: O
authors.initials: O
authors.lastname: Eremin
mesh_terms: D000818:Animals; D001419:Bacteria / Q000472:pathogenicity*; D003093:Colitis, Ulcerative / Q000382:microbiology* / Q000503:physiopathology*; D003424:Crohn Disease / Q000382:microbiology* / Q000503:physiopathology*; D004064:Digestive System / Q000382:microbiology; D004195:Disease Models, Animal; D006801:Humans; D007413:Intestinal Mucosa / Q000166:cytology / Q000382:microbiology / Q000473:pathology; D008221:Lymphoid Tissue / Q000382:microbiology* / Q000473:pathology*; D010539:Permeability; D011157:Population Dynamics; D019936:Probiotics / Q000627:therapeutic use*; D012307:Risk Factors; D014780:Viruses / Q000472:pathogenicity