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Allergic rhinitis (AR) is a common upper airway disease attributed to a variety of risk factors, such as environmental exposures and genetic susceptibility. The commonly observed comorbidity of asthma and AR in the clinic suggests the presence of shared genetic risk factors and biological mechanisms between these diseases. Interleukin () has been indicated to be an important factor driving asthma susceptibility and pathogenesis using both genome-wide association studies and functional studies in model animals. Although previous studies have reported the putative association of this gene with AR, evidence for the association of genetic variations of  with the disease is still missing. To examine whether variations in the  gene confer a genetic risk of AR, a total of 769 patients with AR and 769 age- and sex-matched healthy controls were recruited among Han Chinese residents in the Hubei province, and 14 single-nucleotide polymorphisms (SNPs) spanning the  gene were examined for their association with the risk of AR. The results indicated that five SNPs, which were in a moderate linkage disequilibrium and were located in the 5'-flanking region of , exhibited significant associations with the risk of AR, and these associations were additionally supported by genotypic and haplotypic analyses. Notably, three of the five  SNPs have been previously reported to exhibit genome-wide associations with asthma, and their alleles were also revealed to confer an increased risk of AR in the present study. In summary, the results of the current study suggested that certain variations in the  gene represent a potential risk for AR, and indicated a shared genetic basis between AR and asthma.

Single‑nucleotide polymorphisms and haplotypes in the interleukin‑33 gene are associated with a risk of allergic rhinitis in the Chinese population