Abstract
BackgroundCeliac disease (CD) is a chronic disorder characterized by a pathological inflammatory response after exposure to gluten in genetically susceptible individuals. The HLA complex accounts for less than half of the genetic component of the disease, and additional genes must be implicated. Interleukin-10 (IL-10) is an important regulator of mucosal immunity, and several reports have described alterations of IL-10 levels in celiac patients. The IL-10 gene is located on chromosome 1, and its promoter carries several single nucleotide polymorphisms (SNPs) and microsatellites which have been associated to production levels. Our aim was to study the role of those polymorphisms in susceptibility to CD in our population.MethodsA case-control and a familial study were performed. Positions -1082, -819 and -592 of the IL-10 promoter were typed by TaqMan and allele specific PCR. IL10R and IL10G microsatellites were amplified with labelled primers, and they were subsequently run on an automatic sequencer. In this study 446 patients and 573 controls were included, all of them white Spaniards. Extended haplotypes encompassing microsatellites and SNPs were obtained in families and estimated in controls by the Expectation-Maximization algorithm.ResultsNo significant associations after Bonferroni correction were observed in the SNPs or any of the microsatellites. Stratification by HLA-DQ2 (DQA1*0501-DQB1*02) status did not alter the results. When extended haplotypes were analyzed, no differences were apparent either.ConclusionThe IL-10 polymorphisms studied are not associated with celiac disease. Our data suggest that the IL-10 alteration seen in patients may be more consequence than cause of the disease.
Highlights
Celiac disease (CD) is a chronic disorder characterized by a pathological inflammatory response after exposure to gluten in genetically susceptible individuals
Low levels of IL-10 have been found associated with different typical features of celiac disease such as anti-tissue transglutaminase antibodies [4] and studies using recombinant human IL-10 have shown a suppression of gliadin-specific T cell activation [5]
Genotyping CD patients were genotyped for two single nucleotide polymorphisms (SNPs), -1082 (G/A) and -592 (C/A), both located in the proximal promoter of the IL-10 gene
Summary
Celiac disease (CD) is a chronic disorder characterized by a pathological inflammatory response after exposure to gluten in genetically susceptible individuals. Celiac disease (CD) is a chronic inflammatory disorder characterized by a pathological response after exposure to gluten in genetically susceptible individuals [1]. Cytokines characteristic of a Th1 inflammatory response as interferon gamma, are produced by lamina propria T cells isolated from the intestine of CD patients after gluten stimulation [3]. Low levels of IL-10 have been found associated with different typical features of celiac disease such as anti-tissue transglutaminase antibodies [4] and studies using recombinant human IL-10 (rhIL-10) have shown a suppression of gliadin-specific T cell activation [5]. IL-10 knock-out mice develop chronic enterocolitis, and recent trials have investigated the possibility of using IL-10 as therapy in ulcerative colitis patients [6], another chronic inflammatory disease of the intestinal mucosa
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