Physiological Mechanisms Underpinning Heightened Perception of Visceral Afferent Signalling in Irritable Bowel Syndrome

Interoceptive information relating to intestinal activity and environmental changes in the gut lumen is continuously and, generally, subconsciously being relayed to the central nervous system (CNS). Vagal and spinal afferents are likely to act as the primary interrogators of peripheral intestinal signals, and activation of intestinal nociceptors is associated with the central interpretation of visceral pain. For most of us, gut-to-brain communication is not consciously perceived; however, some are acutely aware of these signals. Individuals with irritable bowel syndrome (IBS), a prevalent and heterogeneous functional bowel disorder, exhibit abnormal sensory perception of signals originating in the gut, which presents as abdominal pain. Although central activity is likely to contribute to visceral hypersensitivity, peripheral factors, including immune, paracrine and endocrine molecules, are also likely to play a role in the sensitisation of gut-to-brain signalling in IBS. We have reviewed the evidence of the contributory mechanisms in IBS-associated visceral hypersensitivity and found that stress, sex and enteroendocrine hormones, in addition to immune molecules, are important contributory factors in intestinal afferent sensitisation. Comorbid psychological disorders also appear to influence the likelihood of individuals with IBS exhibiting symptoms consistent with visceral pain hypersensitivity.