The role of inflammation in irritable bowel syndrome (IBS)

Qin Xiang Ng,1,2 Alex Yu Sen Soh,1 Wayren Loke,2 Donovan Yutong Lim,3 Wee-Song Yeo1 1National University Hospital, National University Health System, Singapore; 2MOH Holdings Pte Ltd, Singapore; 3Institute of Mental Health, Singapore Abstract: Irritable bowel syndrome (IBS) is a complex, functional...

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Autores principales: Ng QX, Soh AYS, Loke W, Lim DY, Yeo WS
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Lenguaje:EN
Publicado: Dove Medical Press 2018
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IBS
Acceso en línea:https://doaj.org/article/4b6f79137ef348099ec9533069da7bbb
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spelling oai:doaj.org-article:4b6f79137ef348099ec9533069da7bbb2021-12-02T07:24:23ZThe role of inflammation in irritable bowel syndrome (IBS)1178-7031https://doaj.org/article/4b6f79137ef348099ec9533069da7bbb2018-09-01T00:00:00Zhttps://www.dovepress.com/the-role-of-inflammation-in-irritable-bowel-syndrome-ibs-peer-reviewed-article-JIRhttps://doaj.org/toc/1178-7031Qin Xiang Ng,1,2 Alex Yu Sen Soh,1 Wayren Loke,2 Donovan Yutong Lim,3 Wee-Song Yeo1 1National University Hospital, National University Health System, Singapore; 2MOH Holdings Pte Ltd, Singapore; 3Institute of Mental Health, Singapore Abstract: Irritable bowel syndrome (IBS) is a complex, functional gastrointestinal ­disorder characterized by chronic abdominal pain or discomfort and altered bowel habits. Despite the global prevalence and disease burden of IBS, its underlying pathophysiology remains unclear. Inflammation may play a pathogenic role in IBS. Studies have highlighted the persistence of mucosal inflammation at the microscopic and molecular level in IBS, with increased recruitment of enteroendocrine cells. Substantial overlaps between IBS and inflammatory bowel disease have also been reported. This review thus aimed to discuss the body of evidence pertaining to the presence of mucosal inflammation in IBS, its putative role in the disease process of IBS, and its clinical relevance. Increased mast cell density and activity in the gut may correlate with symptoms of visceral hypersensitivity. As evidenced by patients who develop postinfectious IBS, infective gastroenteritis could cause systemic inflammation and altered microbiome diversity, which in turn perpetuates a cycle of chronic, low-grade, subclinical inflammation. Apart from mucosal inflammation, neuroinflammation is probably involved in the pathophysiology of IBS via the “gut–brain” axis, resulting in altered neuroendocrine pathways and glucocorticoid receptor genes. This gives rise to an overall proinflammatory phenotype and dysregulated hypothalamic–pituitary–adrenal axis and serotonergic (5-HT) functioning, which could, at least in part, account for the symptoms of IBS. Although a definite and reproducible pattern of immune response has yet to be recognized, further research into anti-inflammatories may be of clinical value. Keywords: irritable bowel syndrome, postinfectious, inflammation, microbiomeNg QXSoh AYSLoke WLim DYYeo WSDove Medical Pressarticleirritable bowel syndromeIBSpost-infectiousinflammationmicrobiomePathologyRB1-214Therapeutics. PharmacologyRM1-950ENJournal of Inflammation Research, Vol Volume 11, Pp 345-349 (2018)
institution DOAJ
collection DOAJ
language EN
topic irritable bowel syndrome
IBS
post-infectious
inflammation
microbiome
Pathology
RB1-214
Therapeutics. Pharmacology
RM1-950
spellingShingle irritable bowel syndrome
IBS
post-infectious
inflammation
microbiome
Pathology
RB1-214
Therapeutics. Pharmacology
RM1-950
Ng QX
Soh AYS
Loke W
Lim DY
Yeo WS
The role of inflammation in irritable bowel syndrome (IBS)
description Qin Xiang Ng,1,2 Alex Yu Sen Soh,1 Wayren Loke,2 Donovan Yutong Lim,3 Wee-Song Yeo1 1National University Hospital, National University Health System, Singapore; 2MOH Holdings Pte Ltd, Singapore; 3Institute of Mental Health, Singapore Abstract: Irritable bowel syndrome (IBS) is a complex, functional gastrointestinal ­disorder characterized by chronic abdominal pain or discomfort and altered bowel habits. Despite the global prevalence and disease burden of IBS, its underlying pathophysiology remains unclear. Inflammation may play a pathogenic role in IBS. Studies have highlighted the persistence of mucosal inflammation at the microscopic and molecular level in IBS, with increased recruitment of enteroendocrine cells. Substantial overlaps between IBS and inflammatory bowel disease have also been reported. This review thus aimed to discuss the body of evidence pertaining to the presence of mucosal inflammation in IBS, its putative role in the disease process of IBS, and its clinical relevance. Increased mast cell density and activity in the gut may correlate with symptoms of visceral hypersensitivity. As evidenced by patients who develop postinfectious IBS, infective gastroenteritis could cause systemic inflammation and altered microbiome diversity, which in turn perpetuates a cycle of chronic, low-grade, subclinical inflammation. Apart from mucosal inflammation, neuroinflammation is probably involved in the pathophysiology of IBS via the “gut–brain” axis, resulting in altered neuroendocrine pathways and glucocorticoid receptor genes. This gives rise to an overall proinflammatory phenotype and dysregulated hypothalamic–pituitary–adrenal axis and serotonergic (5-HT) functioning, which could, at least in part, account for the symptoms of IBS. Although a definite and reproducible pattern of immune response has yet to be recognized, further research into anti-inflammatories may be of clinical value. Keywords: irritable bowel syndrome, postinfectious, inflammation, microbiome
format article
author Ng QX
Soh AYS
Loke W
Lim DY
Yeo WS
author_facet Ng QX
Soh AYS
Loke W
Lim DY
Yeo WS
author_sort Ng QX
title The role of inflammation in irritable bowel syndrome (IBS)
title_short The role of inflammation in irritable bowel syndrome (IBS)
title_full The role of inflammation in irritable bowel syndrome (IBS)
title_fullStr The role of inflammation in irritable bowel syndrome (IBS)
title_full_unstemmed The role of inflammation in irritable bowel syndrome (IBS)
title_sort role of inflammation in irritable bowel syndrome (ibs)
publisher Dove Medical Press
publishDate 2018
url https://doaj.org/article/4b6f79137ef348099ec9533069da7bbb
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