ABSTRACT
Background
Allergic rhinitis (AR) is a T helper type 2 (Th2)-mediated upper airways disease in which genetics factors including cytokine genes play a prominent role. Interleukin-33 (IL-33) is a major cytokine for naive T cells polarization into Th2 phenotype as well as enhances the secretion of Th2 cytokines. The aim of the present study was to investigate the relationship between IL-33 single nucleotide polymorphisms (SNPs) and IL-33 serum level with Allergic rhinitis.
Methods
Blood samples were collected from 130 AR patients and 130 healthy individuals. SNPs (rs7044343 C > T, rs1929992 A > G, rs12551256 A > G) of IL-33 gene were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Serum level of IL-33 was measured by enzyme-linked immunosorbent assay (ELISA).
Results
Statistical analysis showed that the TT genotype (OR = 1.996, CI: 1.168–3.412, P = .01), as well as the T allele (OR = 0.675, CI: 0.476–0.957, P = .02) of rs7044343 C > T were significantly associated with reduced risk of AR. In addition, individuals carrying the TT genotype were associated with lower levels of IL-33 compared to subjects with CC and CT genotypes; however, these differences were not statistically significant. No association was found between rs1929992 and rs12551256 variants and risk of AR, but the GG genotype from rs1929992 A > G was associated with increased serum levels of IL-33 in control group (p = .01). Furthermore, serum IL-33 levels were not significantly different between AR patients and healthy controls (p > .05).
Conclusion
Our results suggest that the TT genotype of rs7044343 C > T may act as a protective agent against allergic rhinitis.
Author contribution
Ali Gorgin Karaji was involved in the concept and design of the study. Farhad Salary drafted the manuscript. All authors were involved in acquisition, analysis, and interpretation of the data, and approved the final version.
Conflicts of interest
None of the authors has any potential financial conflicts of interest related to this manuscript.