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Paraoxonase Gene Expression in Pediatric Inflammatory Bowel Disease | OMICS International | Abstract
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Research Article

Paraoxonase Gene Expression in Pediatric Inflammatory Bowel Disease

Razan H Alkhouri*, Susan S Baker, Humaira Hashmi, Wensheng Liu, Robert D Baker and Lixin Zhu
University at Buffalo, Digestive Disease and Nutrition Center, Buffalo, NY, USA
Corresponding Author : Razan H Alkhouri, MD
Digestive Disease and Nutrition Center
University at Buffalo, 219 Bryant street
Buffalo, NY 14222, USA
Tel: 716-878-7793
Fax: 716-888-3842
E-mail: [email protected]
Received February 25, 2014; Accepted June 10, 2014; Published June 17, 2014
Citation: Alkhouri RH, Baker SS, Hashmi H, Liu W, Baker RD, et al. (2014) Paraoxonase Gene Expression in Pediatric Inflammatory Bowel Disease. J Clin Cell Immunol 5:224. doi: 10.4172/2155-9899.1000224
Copyright: © 2014 Alkhouri RH, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Background: Oxidative stress plays a role in the pathogenesis of inflammatory bowel disease (IBD). The Paraoxonase (PON) genes, expressed in the human intestine, are thought to prevent oxidative stress and modulate inflammation. We investigated the effect of IBD and steroids on PON gene. We hypothesized that PON gene expression is decreased in IBD patients and that steroid treatment would return it to normal.
Methods: Pediatric patients diagnosed with IBD, were enrolled and matched to control subjects. For in vitro studies, human epithelial colorectal adenocarcinoma (Caco-2) cells were treated with hydrogen peroxide (H2O2) and dexamethasone. PON genes expression was evaluated by quantitative real-time PCR for both the biopsies and the Caco-2 cells.
Results: PON gene expression was decreased in intestinal biopsies from medication naïve IBD patients when compared to controls (p<0.05). Biopsies from IBD patients on steroids exhibited up regulation of PON gene expression (p<0.05). Caco-2 cells treated with H2O2 had decreased PON gene expression compared to controls (p<0.05). Dexamethasone increased PON gene expression in Caco-2 cells (p<0.05).
Conclusion: Our data suggests that decreased PON expression in IBD patients is a consequence of oxidative stress which plays a role in the pathogenesis of IBD. Further, steroids counteract the effect of oxidative stress by up regulating PON gene expression. PON genes may be targets for the management of intestinal diseases like IBD.


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