Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 455649
Title Alterations in mucosal neuropeptides in patients with irritable bowel syndrome and ulcerative colitis in remission: A role in pain symptom generation?
Author(s) Keszthelyi, D.; Troost, F.J.; Jonkers, D.M.; Helyes, Z.; Hamer, H.M.; Ludidi, S.; Vanhoutvin, S.; Venema, K.; Dekker, J.; Szolcsanyi, J.; Masclee, A.A.
Source European Journal of Pain 17 (2013)9. - ISSN 1090-3801 - p. 1299 - 1306.
DOI https://doi.org/10.1002/j.1532-2149.2013.00309.x
Department(s) Department of Animal Sciences
Publication type Refereed Article in a scientific journal
Publication year 2013
Keyword(s) vanilloid receptor vr1 - gastrointestinal-tract - abdominal-pain - substance-p - axonal-transport - trpv1 receptor - messenger-rna - rectal mucosa - expression - disease
Abstract Background Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder characterized by chronic abdominal pain. The transient receptor potential vanilloid 1 (TRPV1) channel, which is involved in visceral pain signalling, has been shown to be up-regulated in IBS. Activation of TRPV1 leads to the release of neuropeptides, such as somatostatin and substance P (SP). We hypothesized that increased pain perception in IBS could be explained by increased transcription in TRPV1 and/or altered levels of neuropeptides. We therefore assessed the transcription of TRPV1 and the mucosal concentration of somatostatin and SP in IBS in comparison to healthy volunteers and patients with ulcerative colitis (UC) in remission as disease controls, and to ascertain their relationship to pain symptoms. Method Sigmoid colonic mucosal samples were collected from 12 patients with IBS, 34 patients with UC in remission and 9 healthy volunteers, in which groups TRPV1 mRNA levels were determined using quantitative polymerase chain reaction and neuropeptide concentrations by radioimmunoassay. Pain symptom intensity was determined by questionnaires. Results Transcription of TRPV1 as well as the concentration of neuropeptides were significantly higher in IBS, but only the former correlated with pain symptom severity. Conclusion Increased transcription of TRPV1 may provide a possible explanation for pain generation in IBS. While the neuropeptides SP and somatostatin were both found to be increased in IBS, these changes are not sufficient to explain pain generation. Pain generation in IBS is probably explained by a complex redundancy in the regulation of local nociceptive mechanisms, which remains a subject of intensive investigation.
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