| Irritable Bowel Syndrome(IBS) is the most common gastrointestinal disorder seen in primary care and gastroenterology practice, with high prevalence rate, difficult treatment and expensive medical cost The incidence of IBS has seen huge increase over the past several decades, but etiology and pathogenesis of it remain unclear, which have an effect on its diagnosis and therapy. From the 1950s through to fee eady 1980s enhanced gut motility was thougjtit to be the basis for IBS symptoms. The Mure ofdysmotility to explain symptoms of pain eventually led to studies on visceral hypersensitivity in IBS. It was found that wife balloon distention studies of fee fleum and cdorectum, patients wife IBS experience awareness of distension and pain at pressures and volumes feat are significantly lower than in control subjects. Rectal balloon abstention reproduced chara- cteristic symptomsQower abdominal pain, rectal fullness, urgency) in 69% of patients wife IBS. Reproduction of symptoms was more common in fee low-fereshold group(75%) than in fee rwrmal-fereshold patients(53%).Wife the theory of 'immune-noiroendocrine network' , people came to realize the bidirectional interaction occurred between immune system and nervous system Intestinal mast cell activiation, which results from previous enteric infection or intestinal allergy, may play a central role in fee gut hypersensitivity in both motor response andvisceral perception in the irritable bowel syndrome. This occurs through various mediators acting on enteric neurons and smooth muscle cells. Psychological stress may trigger this sensitive alarm system via the brain-gut axis, ft now seems plausible to assume that peripheral MC-nerve interaction creates not only axonal reflexes in the gut, but also generates signals that are forwarded to the CNS to be intergrated with other informational inputs, and that this elicits the appropriate response to changes in the intestine. Several neuropeptides, such as substance P(SP), calcitonin gene-related peptide(CGRP), vasoactive intestinal peptide(VIP) and neurotension, can modulate the activity of mast cells in mucosa and in connective tissue. The nerve-mast cell cross-talk can occur in the absence of an intermediary transducing cell and that the neuropeptide substance P, operating via NK-1 receptors ,is an irnportant mediator of this communication. These findings have implicatkxis for the neuroirnmune signaling cascades that are likely to occur during airways inflammation, intestinal hvpersensitivity, and other conditions in which mast cells feature. The disorder of physiological function in IBS embodied lively the brain-gut axis and the orgarusm-psyck-social medicine' pattern. The purpose of this study was to explore the mechaniems of visceral hypersensMvity irritable bowd syndrome. 1 Mastt(MCs)ofhites1inalmuc(waThe aim of this part is to investigate whether the mast cells (MC) of intestinal mucosa is elevated in DBS, and to eluciate their possible roles in IBS. The biopsies of the terminal ileum, the ileocecal junction (ICJ), the ascending colon, and thesigmoid colon, were stained specifically with histochemistry for the MCs in 15 concols, 16 diantiea-predominant BBS and 12 constipation-predominant IBS. The results were investigated qualitatively and quantitatively by means of color imagine analyzer. The structural relation between MCs and nerves or cells was studied through an electronic microscopy. The results showed the number of the MCs of the tenninal ileum, the ICJ, the ascending colon, was significantly elevated in the D3S(p <0.01). In the same location ,the density of MCs in diarrhea-predominant IBS is higher than the density of Mcs in constipation-predominant IBS . The density of MCs in sigmoid colon has no change. The MCs in IBS have great variations. The MCs were close to nerves which were demonstrated unrnyeUnated nerves, and to plasma cells in lamina propria. The results indicate that MC may play a cental role in the gut hypersentivity in both motor response and visceral perception in the IBS,and that... |
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