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. 2011 Dec;23(12):1092-7.
doi: 10.1111/j.1365-2982.2011.01792.x. Epub 2011 Sep 23.

Pro-inflammatory chemokine C-C motif ligand 16 (CCL-16) dysregulation in irritable bowel syndrome (IBS): a pilot study

Affiliations

Pro-inflammatory chemokine C-C motif ligand 16 (CCL-16) dysregulation in irritable bowel syndrome (IBS): a pilot study

A Y Del Valle-Pinero et al. Neurogastroenterol Motil. 2011 Dec.

Abstract

Background: Irritable bowel syndrome (IBS) is a serious health problem that affects an estimated 10-15% of people worldwide and has economic consequences in the United States of over $30 billion annually. In the US, IBS affects all races and both sexes, with more females than males (2:1) reporting symptoms consistent with IBS. Although the etiology of this functional gastrointestinal disorder is unknown, literature suggests that a subclinical inflammatory component has a role in the etiologic mechanisms underlying IBS. The aim of this study was to evaluate the gene expression of inflammatory biomarkers in patients with and without IBS and among different IBS phenotypes.

Methods: Irritable bowel syndrome patients (n=12) that met Rome III Criteria for IBS longer than 6months were compared with healthy matched controls (n=12). Peripheral whole blood from fasting participants was collected and RNA was extracted. The expression of 96 inflammatory genes was then analyzed using a custom quantitative real-time PCR array.

Key results: CCL-16 gene expression was upregulated by 7.46-fold in IBS patients when compared with controls. CCL-16 was overexpressed by over 130-fold in IBS-constipation patients when compared with both controls and IBS-diarrhea patients.

Conclusions & inferences: These results further suggest a subclinical inflammatory component underlying IBS. To better understand the phenotypic differences in IBS it is important to broaden the study of these inflammatory and other biomarkers.

Trial registration: ClinicalTrials.gov NCT00824941.

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Conflict of interest statement

CONFLICT OF INTEREST

All of the authors have no potential conflicts of interest to disclose. The opinions expressed herein and the interpretation and reporting of these data are the responsibility of the author(s) and in no way should be seen as an official recommendation, interpretation, or policy of the National Institutes of Health or the US Government.

Figures

Figure 1
Figure 1
Inflammatory Gene Expression in IBS patients vs healthy controls. Compares the expression of all 96 genes and PCR controls for IBS patients (n = 12) vs healthy participants (n = 12). CCL-16 fold regulation = 7.46. Boundary = 4.
Figure 2
Figure 2
Inflammatory Gene Expression in constipation-IBS (IBS-C) patients, diarrhea-IBS (IBS-D) patients and healthy controls. Shows the genetic expression for (A) IBS-C patients (n = 4) vs healthy controls (n = 12) (CCL-16 fold regulation = 199.78); (B) IBS-D patients (n = 8) vs healthy controls (n = 12) and, (C) IBS-C vs IBS-D (CCL-16-fold regulation = 138.47). Boundary = 4.

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