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Abstract
It is suggested that IL-23/IL-17 axis and single nucleotide polymorphisms (SNPs) of IL23R may have crucial role in pathogenesis of Crohn’s disease (CD). Thus, we sought to assess the IL23R SNPs contribution to susceptibility and phenotype of CD. We recruited 117 CD subjects and 117 controls from Poland and 30 CD subjects and 30 controls from Bosnia and Herzegovina (B&H). Two common IL23R SNPs: rs1004819, rs7517847 were genotyped using TaqMan SNP assays. In the Polish population it was found that allele rs1004819: A increases the risk of CD, while allele rs7517847: A is protective against disease development. In Poles the co-carriage of two IL23R risk genotypes was associated with increased risk of CD. A significantly increased risk of CD early onset was observed in Poles carrying at least one rs7517847: G allele. It was also found that IL23R SNPs may be associated with structuring/penetrating CD behavior, as alleles rs1004819: A and rs7517847: G were significantly less frequent in patients without complications, from Poland and B&H, respectively. Allele rs1004819: A was also significantly more frequent in Poles with penetrating CD. These results confirm IL23R SNPs contribution to CD susceptibility in the Polish population and suggest their impact on early age of onset and more severe disease course.
Highlights
Crohn’s disease (CD) is an incurable chronic autoimmune disorder determined by environmental, immunological and genetic factors, characterized by remitting and relapsing inflammation that may occur anywhere along the length of the gastrointestinal tract (GIT) [1,2].Recently, the crucial role of the interleukin 23 (IL-23) signaling pathway (IL-23/IL-17 axis) in CD pathogenesis has been suggested
According to the leading hypothesis the chronic intestinal inflammation is stimulated by pro-inflammatory cytokines including IL-17A, IL-17F, IL-21, and IL-22 produced by activated Th17 (CD4+) lymphocytes [3,4]
All analyzed single nucleotide polymorphisms (SNPs) were in Hardy-Weinberg equilibrium (HWE), both in CD subjects and controls
Summary
The crucial role of the interleukin 23 (IL-23) signaling pathway (IL-23/IL-17 axis) in CD pathogenesis has been suggested. According to the leading hypothesis the chronic intestinal inflammation is stimulated by pro-inflammatory cytokines including IL-17A, IL-17F, IL-21, and IL-22 produced by activated Th17 (CD4+) lymphocytes [3,4]. The essential role of IL-23 and Th17 lymphocytes activation for the induction of chronic intestinal inflammation was demonstrated in animal models [5,6]. It was showed that Th17-related cytokines: IL-17 and IL-22 serum levels are increased in CD and correlates with disease activity [7,8,9,10].
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