Neuroendocrine stimulation of mucosal immune cells in inflammatory bowel disease

Crohn's disease and ulcerative colitis are the major inflammatory bowel diseases (IBD) in humans. With the incidence of increasing world-wide, it currently affects 4 million people in Europe and in the USA. It is an idiopathic, chronic relapsing intestinal disorder of complex pathogenesis. The etiology of both diseases remains unknown, but recent data suggest that they appear in genetically predisposed individuals, because of an exaggerated mucosal immune response to commensal microbiota present in the gut. There is increasing evidence for an alteration of the immune regulation mechanisms in patients, with mucosal T lymphocytes playing a crucial role in the pathogenic events leading to tissue damage. It is clear that the disease is the result of environmental factors acting on genetically predisposed individuals. In humans, psychological trauma, stress or depression, have been involved as precipitating or relapsing factors of the disease, although this link remains elusive. However, several published works using colitis animal models subjected to stress conditions, have given consistent proof as to the molecular link between emotional stress, increase in epithelial permeability, alteration of the gut microflora composition and activation of pre-sensitized T lymphocytes. Gaining knowledge of the cross talk between components of the brain - gut - immune system axis may be fruitful in the design of future therapeutic approaches, such as the use of vasointestinal peptide (VIP) in this pathology.