{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T17:24:40Z","timestamp":1791393880586,"version":"4.3.3"},"reference-count":36,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2014,2,19]],"date-time":"2014-02-19T00:00:00Z","timestamp":1392768000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neurogastroenterology Motil"],"published-print":{"date-parts":[[2014,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>In this issue of <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>eurogastroenterology and <jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>otility, Dr Ewa Wilcz\u2010Villega and colleagues report low expression of E\u2010cadherin, a tight junction protein involved in the regulation of paracellular permeability, in the colonic mucosa of patients with the irritable bowel syndrome (<jats:styled-content style=\"fixed-case\">IBS<\/jats:styled-content>) with predominance of diarrhea (<jats:styled-content style=\"fixed-case\">IBS<\/jats:styled-content>\u2010D) or alternating symptoms (<jats:styled-content style=\"fixed-case\">IBS<\/jats:styled-content>\u2010A). These findings constitute an improvement in our knowledge of epithelial barrier disruption associated with <jats:styled-content style=\"fixed-case\">IBS<\/jats:styled-content>. There is mounting evidence to indicate that a compromised epithelial barrier is associated with low\u2010grade immune activation and intestinal dysfunction in at least a proportion of <jats:styled-content style=\"fixed-case\">IBS<\/jats:styled-content> patients. During the last 10\u00a0years of research, much interest has focused on the increase in the number of different types of immune cells in the gut mucosa of <jats:styled-content style=\"fixed-case\">IBS<\/jats:styled-content> patients including: mast cells, T lymphocytes, and other local cells such as enteroendocrine cells. The inflammatory mediators released by these cells or other luminal factors could be at the origin of altered epithelial barrier functions and enteric nervous system signaling, which lead to gut hypersensitivity. A current conceptual framework states that clinical symptoms of <jats:styled-content style=\"fixed-case\">IBS<\/jats:styled-content> could be associated with structural and functional abnormalities of the mucosal barrier, highlighting the crucial importance of elucidating the contributory role of epithelial barrier defects in the pathogenesis of <jats:styled-content style=\"fixed-case\">IBS<\/jats:styled-content>. More importantly, disruption of the epithelial barrier could also participate in the generation of persistent abdominal pain and discomfort mimicking <jats:styled-content style=\"fixed-case\">IBS<\/jats:styled-content> in patients with inflammatory bowel diseases considered in remission. This mini review gives a brief summary of clinical and experimental evidence concerning the mechanisms underlying epithelial barrier defects in <jats:styled-content style=\"fixed-case\">IBS<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/nmo.12315","type":"journal-article","created":{"date-parts":[[2014,2,19]],"date-time":"2014-02-19T06:27:45Z","timestamp":1392791265000},"page":"296-302","source":"Crossref","is-referenced-by-count":137,"title":["Tight junctions and <scp>IBS<\/scp> \u2010 the link between epithelial permeability, low\u2010grade inflammation, and symptom generation?"],"prefix":"10.1111","volume":"26","author":[{"given":"T.","family":"Piche","sequence":"first","affiliation":[{"name":"Department of Gastroenterology CHU Nice France"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2014,2,19]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1136\/gut.47.6.804"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2036.2004.02284.x"},{"key":"e_1_2_8_4_1","doi-asserted-by":"crossref","first-page":"2956","DOI":"10.1111\/j.1572-0241.1999.01444.x","article-title":"Intestinal permeability as a predictor of clinical course in Crohn's disease","volume":"94","author":"D'Inca R","year":"1999","journal-title":"Am J Gastroenterol"},{"key":"e_1_2_8_5_1","first-page":"254","article-title":"Structural abnormalities of jejunal epithelial cell membranes in celiac sprue","volume":"43","author":"Madara JL","year":"1980","journal-title":"Lab Invest"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2009.12.049"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1136\/gut.2007.140210"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1136\/gut.2007.140806"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.1038\/ajg.2009.700"},{"key":"e_1_2_8_10_1","doi-asserted-by":"publisher","DOI":"10.1038\/ajg.2011.257"},{"key":"e_1_2_8_11_1","doi-asserted-by":"publisher","DOI":"10.1053\/gast.2002.33579"},{"key":"e_1_2_8_12_1","doi-asserted-by":"publisher","DOI":"10.1136\/gut.2007.127068"},{"key":"e_1_2_8_13_1","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2003.09.028"},{"key":"e_1_2_8_14_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI0215695"},{"key":"e_1_2_8_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)62264-X"},{"key":"e_1_2_8_16_1","doi-asserted-by":"publisher","DOI":"10.1096\/fj.04-3260com"},{"key":"e_1_2_8_17_1","doi-asserted-by":"publisher","DOI":"10.1038\/ajg.2011.86"},{"key":"e_1_2_8_18_1","first-page":"541","article-title":"Mast cells in inflammatory conditions of the gastrointestinal tract","volume":"37","author":"Hiatt RB","year":"1962","journal-title":"Am J Gastroenterol"},{"key":"e_1_2_8_19_1","doi-asserted-by":"publisher","DOI":"10.1053\/gast.2002.37059"},{"key":"e_1_2_8_20_1","doi-asserted-by":"publisher","DOI":"10.1038\/ajg.2011.315"},{"key":"e_1_2_8_21_1","doi-asserted-by":"publisher","DOI":"10.3748\/wjg.v13.45.6041"},{"key":"e_1_2_8_22_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2982.2000.00221.x"},{"key":"e_1_2_8_23_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI29255"},{"key":"e_1_2_8_24_1","doi-asserted-by":"publisher","DOI":"10.1080\/00365520410009410"},{"key":"e_1_2_8_25_1","doi-asserted-by":"publisher","DOI":"10.1136\/gutjnl-2012-302093"},{"key":"e_1_2_8_26_1","doi-asserted-by":"publisher","DOI":"10.1038\/ajg.2011.472"},{"key":"e_1_2_8_27_1","doi-asserted-by":"publisher","DOI":"10.1136\/gut.49.6.743"},{"key":"e_1_2_8_28_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2006.120907"},{"key":"e_1_2_8_29_1","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2003.11.055"},{"key":"e_1_2_8_30_1","doi-asserted-by":"publisher","DOI":"10.1007\/s11033-013-2724-y"},{"key":"e_1_2_8_31_1","doi-asserted-by":"publisher","DOI":"10.1136\/gutjnl-2012-304066"},{"key":"e_1_2_8_32_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.pain.2009.06.017"},{"key":"e_1_2_8_33_1","doi-asserted-by":"publisher","DOI":"10.1038\/ajg.2008.94"},{"key":"e_1_2_8_34_1","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2009.07.005"},{"key":"e_1_2_8_35_1","doi-asserted-by":"publisher","DOI":"10.1038\/ajg.2013.152"},{"key":"e_1_2_8_36_1","doi-asserted-by":"publisher","DOI":"10.1038\/ajg.2013.92"},{"key":"e_1_2_8_37_1","doi-asserted-by":"publisher","DOI":"10.1136\/gut.2003.015867"}],"container-title":["Neurogastroenterology &amp; 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