Extract

To the Editor:

The peroxisome proliferator-activated receptor gamma (PPAR-γ) has been proposed as a key inhibitor of colitis through attenuation of nuclear factor kappa B (NF-κB) activity. Impaired expression of PPAR-gamma in colonic epithelial cells in ulcerative colitis (UC) and increased expression in hypertrophic mesenteric adipose tissue in Crohn's disease (CD) have been reported.1 Recently, it has become controversial whether genetic polymorphism may play a role in the etiology of inflammatory bowel disease (IBD).2,4 However, this is the first study, to our best knowledge, with a larger sample that correlates the PPAR-γ gene expression negatively with disease activity in patients with UC. We measured the PPAR-γ gene expression from rectum biopsies of UC patients from September 2007 to August 2008. All individuals were divided into two groups: 1) active UC (n = 20), and 2) long-term UC remission (n = 20). All individuals were assessed for PPAR-γ and IL-6 mRNA transcripts levels relative to RPLP0 constitutive gene using real-time reverse-transcription polymerase chain reaction (RT-PCR) using LNA TaqMan probes from Roche (Nutley, NJ) in combination with target gene-specific primers PPAR-γ forward 5′-gacctgaaacttcaagagtaccaaa-3′ and reverse 5′-tgaggcttattgtagagctgagtc-3′; IL-6 5′-gcccagctatgaactccttct-3′, 5′-gaaggcagcaggcaacac-3′; and RPLP0 5′-acagggcgacctggaagt-3′, 5′-ggatctgctgcatctgctt-3′ for normalization.

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