Recently, a -105G>A promoter polymorphism coding for
selenoprotein S (SELS) has been shown to increase proinflammatory
cytokine expression. We, therefore, analyzed SELS expression and potential phenotypic consequences of the -105G>A polymorphism in patients with
inflammatory bowel disease (IBD). SELS
mRNA was measured by quantitative polymerase chain reaction (PCR) in intestinal epithelial cells (IEC) after stimulation with proinflammatory
cytokines and in human colonic biopsies of IBD patients as well as in murine models of
ileitis and murine cytomegalovirus (MCMV)
colitis. Genomic
DNA from 563 individuals (
Crohn's disease: n = 205;
ulcerative colitis: n = 154; controls: n = 204) was analyzed for the presence of the SELS-105G>A polymorphism and the three
nucleotide-binding oligomerization domain-containing
protein 2 (NOD2)/caspase recruitment domain-containing
protein 15 (CARD15) variants p.Arg702Trp, p.Gly908Arg and p.Leu1007fsX1008. SELS
mRNA expression was increased in IEC after stimulation with proinflammatory
cytokines, while its expression was not significantly altered in murine
ileitis and MCMV
colitis and in inflamed ileal and colonic lesions in IBD patients compared with normal controls. The SELS-105G>A polymorphism was observed with similar frequencies in IBD patients and controls and was not associated with a certain disease phenotype or serum
tumor necrosis factor alpha (
TNF-alpha) levels in these patients. Medium serum
TNF-alpha was 1.27 pg/ml in IBD patients, while none of the controls had
TNF-alpha concentrations above the detection threshold (P < 0.0001). SELS
mRNA expression is upregulated by proinflammatory
cytokines in IECs but the SELS-105G>A polymorphism is not associated with IBD susceptibility and does not contribute to a certain disease phenotype or increased
TNF-alpha levels in IBD patients.