Article Summary Psychoneuroimmunology of Irritable Bowel Syndrome

This paper shall summarize the findings of a review article (Arebi, Gurmany, Bullas, Hobson, Stagg, Kamm, 2008) that discussed the relationship of psychoneuroimmunology to the pathophysiology of Irritable Bowel Syndrome (IBS). Irritable Bowel Syndrome (IBS) is a chronic functional disorder of the gastrointestinal tract, which affects about 10-15% of the world’s population. The characteristic features of the disease are intermittent bouts of abdominal pain, accompanied by abnormal stool frequency and/or consistency. Two main pathophysiologic mechanisms for IBD have been proposed: the first is the gut-directed model, which implicates enteric bacteria,immune activation, visceral hypersensitivity and gut dysmotility to interact and culminate in producing abdominal pain and constipation or diarrhea. The second is the brain-directed model, which discusses psychoneuroimmunologic factors leading to development of IBS. There is a strong association between psychological disorders and IBS. Previous psychological trauma, depression, anxiety and personality disorders are frequent among IBS patients. IBS patients have increased activity in brain areas for affect and attention, which are also stimulated by noxious stimuli. Upon colorectal distention, they report feeling abdominal pain and the urge to defecate at much lower levels of distention compared to non-IBS subjects. At the same time, visceral neuro-sensory activity in IBS patients is normal. This suggests that IBS patients are hypersensitive to visceral stimuli, feeling pain even with innocuous levels of colonic distention. Studies have shown an association between symptoms of anxiety and depression and higher abdominal pain ratings, despite normal rectal sensory thresholds. A plausible theory suggested by these results is that visceral sensory neuronal impulses in the spinal cord are enhanced to heighten pain perception by cortical signals that stem from psychological distress. Colonic biopsies of IBS patients have shown an increased number of inflammatory and immune cells, as well as the presence of inflammatory cytokines, such as histamine, IL-1 and -6, in the gut wall. These cytokines directly increase visceral sensation and symptom severity of IBS by stimulating autonomic neurons. The increase in cytokine levels in IBS is attributed to genetic factors, such as a deficiency in the production of anti-inflammatory proteins such as IL-10. Previous gut infections induce an immunologic response and lead to cytokine release, which can continue un-mitigated in the absence of anti-inflammatory regulation. Furthermore, studies have shown that the presence of anxiety is associated with a heightened immunologic response to infection in the gut. Psychological stress also induces an increase in the permeability of gut epithelium by unknown mechanisms, permitting greater interaction between immune cells and gut bacteria, and thus more inflammation leading to onset of pain and diarrhea. This implies that individuals with a stressful personality and a genetic deficiency in anti-inflammatory regulation, would be likely to develop IBS after minor gut infections or upon psychological stress that normal individuals recover from completely. Animal studies have helped clarify the apparent interaction between the neural system, the immune system and enteric bacteria. Gut bacteria prevent infection

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