Toll-like receptor mRNA expression is selectively increased in the colonic mucosa of two animal models relevant to irritable bowel syndrome

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dc.contributor.author McKernan, Declan P.
dc.contributor.author Nolan, Aoife
dc.contributor.author Brint, Elizabeth K.
dc.contributor.author O'Mahony, Siobhain M.
dc.contributor.author Hyland, Niall P.
dc.contributor.author Cryan, John F.
dc.contributor.author Dinan, Timothy G.
dc.date.accessioned 2010-02-08T13:40:29Z
dc.date.available 2010-02-08T13:40:29Z
dc.date.issued 2009-11-09
dc.identifier.citation McKernan DP, Nolan A, Brint EK, O’Mahony SM, Hyland NP, et al. (2009) Toll-Like Receptor mRNA Expression Is Selectively Increased in the Colonic Mucosa of Two Animal Models Relevant to Irritable Bowel Syndrome. PLoS ONE 4(12): e8226. doi:10.1371/journal.pone.0008226 en
dc.identifier.volume 4 en
dc.identifier.issued 12 en
dc.identifier.startpage e8226 en
dc.identifier.issn 1932-6203
dc.identifier.uri http://hdl.handle.net/10468/111
dc.identifier.doi 10.1371/journal.pone.0008226
dc.description.abstract Background: Irritable bowel syndrome (IBS) is largely viewed as a stress-related disorder caused by aberrant brain-gut– immune communication and altered gastrointestinal (GI) homeostasis. Accumulating evidence demonstrates that stress modulates innate immune responses; however, very little is known on the immunological effects of stress on the GI tract. Toll-like receptors (TLRs) are critical pattern recognition molecules of the innate immune system. Activation of TLRs by bacterial and viral molecules leads to activation of NF-kB and an increase in inflammatory cytokine expression. It was our hypothesis that innate immune receptor expression may be changed in the gastrointestinal tract of animals with stressinduced IBS-like symptoms. Methodology/Principal Findings: In this study, our objective was to evaluate the TLR expression profile in the colonic mucosa of two rat strains that display colonic visceral hypersensivity; the stress-sensitive Wistar-Kyoto (WKY) rat and the maternally separated (MS) rat. Quantitative PCR of TLR2-10 mRNA in both the proximal and distal colonic mucosae was carried out in adulthood. Significant increases are seen in the mRNA levels of TLR3, 4 & 5 in both the distal and proximal colonic mucosa of MS rats compared with controls. No significant differences were noted for TLR 2, 7, 9 & 10 while TLR 6 could not be detected in any samples in both rat strains. The WKY strain have increased levels of mRNA expression of TLR3, 4, 5, 7, 8, 9 & 10 in both the distal and proximal colonic mucosa compared to the control Sprague-Dawley strain. No significant differences in expression were found for TLR2 while as before TLR6 could not be detected in all samples in both strains. Conclusions: These data suggest that both early life stress (MS) and a genetic predisposition (WKY) to stress affect the expression of key sentinels of the innate immune system which may have direct relevance for the molecular pathophysiology of IBS. en
dc.description.sponsorship Science Foundation Ireland (Centre for Science and Technology (CSET)); GlaxoSmithKline, United Kingdom en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher Public Library of Science en
dc.rights ©2009 McKernan et al. en
dc.rights.uri http://creativecommons.org/licenses/by/2.5/ en
dc.subject Toll-like receptors en
dc.subject Irritable bowel syndrome en
dc.subject Immunologic receptors en
dc.subject.lcsh Gastrointestinal system -- Diseases en
dc.title Toll-like receptor mRNA expression is selectively increased in the colonic mucosa of two animal models relevant to irritable bowel syndrome en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother Declan P. McKernan, Laboratory of Neurogastroenterology, Alimentary Pharmabiotic Centre, University College Cork, Cork, Ireland. en
dc.internal.authorcontactother Aoife Nolan, Laboratory of Neurogastroenterology, Alimentary Pharmabiotic Centre, University College Cork, Cork, Ireland. en
dc.internal.authorcontactother Elizabeth K. Brint, Laboratory of Neurogastroenterology, Alimentary Pharmabiotic Centre, University College Cork, Cork, Ireland. E-mail: e.brint@ucc.ie en
dc.internal.authorcontactother Siobhain M. O’Mahony, Laboratory of Neurogastroenterology, Alimentary Pharmabiotic Centre, University College Cork, Cork, Ireland. E-mail: somahony@ucc.ie en
dc.internal.authorcontactother Niall P. Hyland, Laboratory of Neurogastroenterology, Alimentary Pharmabiotic Centre, University College Cork, Cork, Ireland. E-mail: n.hyland@ucc.ie en
dc.internal.authorcontactother John F. Cryan, Laboratory of Neurogastroenterology, Alimentary Pharmabiotic Centre, University College Cork, Cork, Ireland. E-mail: j.cryan@ucc.ie en
dc.internal.authorcontactother Timothy G. Dinan, Laboratory of Neurogastroenterology, Alimentary Pharmabiotic Centre, University College Cork, Cork, Ireland. E-mail: t.dinan@ucc.ie en
dc.internal.availability Full text available en
dc.description.version Published Version en
dc.contributor.funder Science Foundation Ireland en
dc.contributor.funder GlaxoSmithKline, United Kingdom en
dc.description.status Peer reviewed en
dc.identifier.journaltitle PLoS ONE en
dc.internal.IRISemailaddress n.hyland@ucc.ie en


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