Pathogenesis of IBS: role of inflammation, immunity and neuroimmune interactions

Abstract

IBS is one of the most common functional gastrointestinal disorders worldwide and is thought to be the result of disturbed neural function along the brain-gut axis. The mechanisms behind this disturbance are not clear, but important roles for low-grade inflammation and immunological alterations in the development of symptoms compatible with IBS have become evident. The development of long-standing gastrointestinal symptoms after infectious gastroenteritis and patients with IBD in remission frequently having functional gastrointestinal symptoms support this hypothesis. An increased innate immune activity in the intestinal mucosa and in blood is found in subpopulations of patients with IBS. Mast cells and monocytes seem to be particularly important. In addition, studies have demonstrated that IBS may be associated with an activated adaptive immune response. Increased epithelial barrier permeability and an abnormal gut flora might lead to increased activation of the intestinal immune system. Functional and anatomical evidence for abnormal neuroimmune interactions has been found in patients with IBS. The link between immune alterations and severity of gastrointestinal symptoms and the positive effect of anti-inflammatory treatments in IBS further highlight the relevance of neuroimmune interactions in this condition.