Alterations in mucosal neuropeptides in patients with irritable bowel syndrome and ulcerative colitis in remission: A role in pain symptom generation?

D. Keszthelyi*, F.J. Troost, D.M.A.E. Jonkers, Z. Helyes, H.M.H. Hamer, S. Ludidi, S.A.L.W. Vanhoutvin, K. Venema, J. Dekker, J. Szolcsanyi, A.A.M. Masclee

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

BACKGROUND: Irritable bowel syndrome (IBS) is a functional disorder characterized by chronic abdominal pain. The transient receptor potential vanilloid 1 (TRPV1) channel, which is involved in visceral signalling, has been shown to be up-regulated in IBS. Activation of to the release of neuropeptides, such as somatostatin and substance P hypothesized that increased pain perception in IBS could be explained by increased transcription in TRPV1 and/or altered levels of neuropeptides. therefore assessed the transcription of TRPV1 and the mucosal somatostatin and SP in IBS in comparison to healthy volunteers and ulcerative colitis (UC) in remission as disease controls, and to relationship to pain symptoms. METHOD: Sigmoid colonic mucosal samples collected from 12 patients with IBS, 34 patients with UC in remission healthy volunteers, in which groups TRPV1 mRNA levels were determined quantitative polymerase chain reaction and neuropeptide concentrations radioimmunoassay. Pain symptom intensity was determined by RESULTS: Transcription of TRPV1 as well as the concentration of were significantly higher in IBS, but only the former correlated with symptom severity. CONCLUSION: Increased transcription of TRPV1 may possible explanation for pain generation in IBS. While the neuropeptides
Original languageEnglish
Pages (from-to)1299-1306
Number of pages8
JournalEuropean Journal of Pain
Volume17
Issue number9
DOIs
Publication statusPublished - Oct 2013

Keywords

  • VANILLOID RECEPTOR VR1
  • GASTROINTESTINAL-TRACT
  • ABDOMINAL-PAIN
  • SUBSTANCE-P
  • AXONAL-TRANSPORT
  • TRPV1 RECEPTOR
  • MESSENGER-RNA
  • RECTAL MUCOSA
  • EXPRESSION
  • DISEASE

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