Document Detail


Serum and colonic mucosal immune markers in irritable bowel syndrome.
MedLine Citation:
PMID:  22158028     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: Low-grade colonic mucosal inflammation has been postulated to have an important role in the pathophysiology of irritable bowel syndrome (IBS). The objectives of this study were (i) to identify serum and tissue-based immunological and neuroendocrine markers associated with mucosal inflammation in male (M) and female (F) patients with non-post-infectious IBS (non-PI-IBS) compared with healthy controls and (ii) to assess possible correlations of such markers with IBS symptoms.
METHODS: Sigmoid mucosal biopsies were obtained from 45 Rome II positive IBS patients without a history of PI-IBS (26 F, 35.5% IBS-C, 33.3% IBS-D, 31.1% IBS-A/M) and 41 healthy controls (22 F) in order to measure immunological markers (serum cytokine levels, colonic mucosal mRNA levels of cytokines, mucosal immune cell counts) and neuroendocrine markers associated with mucosal inflammation (corticotropin releasing factor- and neurokinin (NK)-related ligands and receptors, enterochromaffin cells). Symptoms were measured using validated questionnaires.
RESULTS: Of all the serum and mucosal cytokines measured, only interleukin-10 (IL-10) mRNA expression showed a group difference, with female, but not male, patients showing lower levels compared with female controls (18.0±2.9 vs. 29.5±4.0, P=0.006). Mucosal mRNA expression of NK-1 receptor was significantly lower (1.15±0.19 vs. 2.66±0.56, P=0.008) in female, but not male, patients compared with healthy controls. No other significant differences were observed.
CONCLUSIONS: Immune cell counts and levels of cytokines and neuropeptides that are associated with inflammation were not significantly elevated in the colonic mucosa of non-PI-IBS patients, and did not correlate with symptoms. Thus, these findings do not support that colonic mucosal inflammation consistently has a primary role in these patients. However, the finding of decreased IL-10 mRNA expression may be a possible biomarker of IBS and warrants further investigation.
Authors:
Lin Chang; Mopelola Adeyemo; Iordanis Karagiannides; Iordanis Karagiannidis; Elizabeth J Videlock; Collin Bowe; Wendy Shih; Angela P Presson; Pu-Qing Yuan; Galen Cortina; Hua Gong; Sharat Singh; Arlene Licudine; Minou Mayer; Yvette Tache; Charalabos Pothoulakis; Emeran A Mayer
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-12-13
Journal Detail:
Title:  The American journal of gastroenterology     Volume:  107     ISSN:  1572-0241     ISO Abbreviation:  Am. J. Gastroenterol.     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-02-06     Completed Date:  2012-04-10     Revised Date:  2012-04-12    
Medline Journal Info:
Nlm Unique ID:  0421030     Medline TA:  Am J Gastroenterol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  262-72     Citation Subset:  IM    
Affiliation:
Center for Neurobiology of Stress, University of California, Los Angeles, California 90095-7378, USA. linchang@ucla.edu
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Biological Markers / metabolism*
Colon / immunology,  metabolism*,  pathology
Cytokines / metabolism
Female
Humans
Interleukin-10 / metabolism
Intestinal Mucosa / immunology,  metabolism*,  pathology
Irritable Bowel Syndrome / immunology,  metabolism*,  pathology
Male
Middle Aged
Questionnaires
Receptors, Neurokinin-1 / metabolism
Sex Factors
Grant Support
ID/Acronym/Agency:
DK047343/DK/NIDDK NIH HHS; P01 DK33506/DK/NIDDK NIH HHS; P50 DK064539-10/DK/NIDDK NIH HHS; P50DK64539/DK/NIDDK NIH HHS; R01 DK048351-14/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Cytokines; 0/Receptors, Neurokinin-1; 130068-27-8/Interleukin-10
Comments/Corrections
Comment In:
Am J Gastroenterol. 2012 Feb;107(2):273-5   [PMID:  22306945 ]
Erratum In:
Am J Gastroenterol. 2012 Mar;107(3):492
Note: Karagiannidis, Iordanis [corrected to Karagiannides, Iordanis]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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