Background/aims: Preeclampsia (PE) is a systemic inflammatory response syndrome involving varieties of cytokines, and previous studies have shown that IL-33 and its receptor IL-1RL1 play pivotal roles in the development of it. As a polygenetic hereditary disease, it is necessary to study the gene analysis for PE. Therefore, the present study was to determine whether IL-33 rs3939286 and IL-1RL1 rs13015714 associated with susceptibility to PE in Chinese Han women.
Methods: 1,031 PE patients and 1,298 controls were enrolled and the genotyping for rs3939286 in IL-33 and rs13015714 in IL-1RL1 was performed by TaqMan allelic discrimination real-time PCR. Hardy-Weinberg equilibrium (HWE) was examined to ensure the group representativeness and Pearson's chi-square test was used to compare the differences in genetic distributions between the two groups.
Results: No significant differences in genotypic and allelic frequencies of the two polymorphisms loci were observed between cases and controls. There were also no significant differences in genetic distributions between mild/severe and early/late-onset PE and control groups.
Conclusion: Although our data suggested that the polymorphisms of IL-33 rs3939286 and IL-1RL1 rs13015714 might not be critical risk factors for PE in Chinese Han women, the results need to be validated in different nations.
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http://dx.doi.org/10.1159/000443083 | DOI Listing |
Int J Mol Sci
December 2024
Department of Anatomy, "Iuliu Hatieganu" University of Medicine and Pharmacy, 400006 Cluj-Napoca, Romania.
Urticaria is a debilitating skin condition affecting up to 20% of the global population, characterized by erythematous, maculopapular lesions and significant quality of life impairment. This study focused on the role of interleukin 33 (IL-33) and its polymorphisms, particularly SNP , in chronic spontaneous urticaria (CSU). Using demographic, clinical, and laboratory data from CSU patients and controls, we estimated allele and genotype frequencies, Hardy-Weinberg equilibrium condition, and serum IL-33 levels, using unconditional binomial logistic regression for association analysis.
View Article and Find Full Text PDFCytokine
February 2025
Department of Periodontology and Oral Mucosa, The Second Affiliated Hospital of Harbin Medical University, Harbin, China; Heilongjiang Provincial Key Laboratory of Hard Tissue Development and Regeneration, The Second Affiliated Hospital of Harbin Medical University, Harbin, China. Electronic address:
BMC Res Notes
November 2024
Department of Biology, Zand Institute of Higher Education, Shiraz, Iran.
Sci Rep
October 2024
Department of Otorhinolaryngology, Head and Neck Surgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Chronic rhinosinusitis (CRS) is a prevalent inflammatory airway disease affecting over 10% of the global population, leading to considerable socio-economic impacts, especially in developing countries. The pathogenesis of CRS is multifactorial, involving potential contributions from both genetic and environmental factors. While the influence of allergic and autoimmune diseases on CRS has been observed, the causal relationships between these diseases and CRS remain unclear.
View Article and Find Full Text PDFClin Exp Allergy
December 2024
Centre for Respiratory Research, National Institute for Health Research Nottingham Biomedical Research Centre, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, UK.
Introduction: The interleukin-33/interleukin-1 receptor-like-1 (IL-33/IL1RL1) signalling pathway is implicated in asthma pathogenesis, with IL1RL1 nonsynonymous genetic polymorphisms associated with disease risk. We aimed to determine these variants' effect on IL1RL1 signalling induced by different IL33 isoforms thought to be elevated in the asthmatic airway.
Method: In a project funded by GSK plc, which has developed an IL-33 receptor inhibitor for asthma treatment, human embryonic kidney 293 (HEK293) cells expressing secreted embryonic alkaline phosphatase (SEAP) driven by a nuclear factor kappa-beta (NF-κB) promoter, were transiently transfected with IL1RL1, containing one of four extracellular and Toll/interleukin 1 receptor (TIR) domain haplotypes.
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