From Sensitivity to Symptoms: Understanding the Intricate Pathways of Visceral Hypersensitivity in Irritable Bowel Syndrome

Abstract

A significant contributing factor to gastrointestinal diseases with mild or moderate symptoms is visceral hypersensitivity, which is present in IBS (irritable bowel syndrome). IBS is characterized by bloating, bowel irregularities, and pain or irritation in the abdomen. Irritable bowel syndrome is hypothesized to be caused by increased epithelial hyperpermeability, inflammation, dysbiosis, altered brain-gut interactions, epigenetics, genetics, and visceral hypersensitivity (VH). However, the specific pathophysiology is yet unknown. Visceral hypersensitivity to luminal stimuli results from many pathways at the peripheral, spinal, and supraspinal levels that lead to sensitizing receptors in visceral pain. The primary afferents of the vagus nerve and spinal nerve both innervate the gut viscera. The intestine's intrinsic enteric nervous system (ENS), which contains intrinsic primary afferent neurons, integrates gut motility and peristalsis (IPAN). In IBS patients, a persistently overactive afferent from the colon to the spinal cord causes secondary somatic hypersensitivity. Both human and animal models of visceral hypersensitivity have been used to investigate this process. A breach in the gut barrier can also result in systemic abnormalities and gastrointestinal dysfunction. According to clinical research, micro-RNA expression increases in the colon tissue in IBS models. It has been found that these microRNAs help IBS patients' epigenetic and genetic events. The fundamental elements that link gut somatic and visceral systems with IBS are covered in this review. The literature review highlights various phenomena of signals originating from the colon that affect the GIT of IBS patients, such as changes in microRNA expression, changes in intestine permeability, and hypersensitivity in the GIT, as well as experimental exploration of VH in inflammatory bowel syndrome.