IBD - Diagnosis and Treatment

IBD – diagnosis and treatment
 

Introduction
The normal intestinal epithelium is not inflamed despite close contact with a high density of commensal organisms which would elicit inflammation when entering the body by other routes (1). Intestinal epithelial cells serve as a barrier between the body and viruses, bacteria and parasites present in the intestinal lumen. Rather than being a passive barrier, the intestinal epithelium is an active participant in the mucosal immune response through antigen processing and presentation, secretion of cytokines, and recruitment of inflammatory cells in response to pathogens and their products (2). The gastrointestinal-associated lymphoid tissue (GALT) is the largest and most complex immunological organ of the body and must be capable of mounting a protective immune response to pathogens, whilst maintaining tolerance to harmless environmental antigens such as commensal bacteria and food. The breakdown of this tolerance is a key factor in the development of chronic intestinal inflammation.

Inflammatory bowel disease (IBD)
In human beings, the term inflammatory bowel disease (IBD) encompasses the two distinct entities of Crohn’s disease and ulcerative colitis. 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 human IBD (3). Also the 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 (3). […]