부산대학교 도서관

To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1365-2796.2008.01962.x Byline: C. D. Packey (1), R. B. Sartor (2) Keywords: gastroenterology; genetics; inflammation Abstract: Abstract Enteric microbiota can contribute to Crohn's disease and ulcerative colitis in several ways. Pathogenic or functionally altered commensal bacteria with increased mucosal adherence, invasion and intracellular persistence can activate pathogenic T cells and chronic intestinal inflammation. Compositional changes in intestinal microbiota can lead to decreased protective and increased aggressive species. Genetic polymorphisms resulting in increased mucosal permeability, decreased microbial killing, ineffective clearance of bacteria, biased TH1 and TH17 immune responses and loss of immunological tolerance are probably key contributors to IBD. Future therapies for these heterogeneous diseases should be individualized based on the patient-specific subset. Author Affiliation: From the Departments of(1)Medicine (2)Microbiology and Immunology, Program of Digestive Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA Article note: R. Balfour Sartor, UNC Department of Medicine/GI, CB #7032, Room 7309, Biomolecular Building, Chapel Hill, NC 27599 7032, USA., (fax: (919) 843 6899; e-mail: rbs@med.unc.edu).