Abstract
BackgroundAllergic rhinitis (AR) is a chronic inflammatory disease of the nasal mucosa, involving a complex interaction between genetic and environmental factors. Evidence suggests that polymorphisms in the gene coding for mitochondrial ribosomal protein L4 (MRPL4), located in close proximity to intercellular adhesion molecule-1 (ICAM-1) gene on chromosome location 19p13.2, may influence the risk factor for the development of AR.ObjectiveThe aim of our study was to investigate any association between AR susceptibility and polymorphisms in ICAM-1 gene, as well as associations between AR risk and polymorphisms in MRPL4, nuclear factor-kappaB (NF-κB) and tumor necrosis factor alpha(TNF-α) genes, associated with ICAM-1 expression.MethodsA cohort of 414 patients with AR and 293 healthy controls was enrolled from the Han Chinese population in Beijing, China. Blood was drawn for DNA extraction and total serum immunoglobulin E (IgE). A total of 14 single nucleotide polymorphisms (SNPs) in ICAM-1, NF-κB, TNF-α, and MRPL4 genes were selected using the CHB genotyping data from the International Haplotype Mapping (HapMap) and assessed for differences in frequencies of the alleles and genotypes between the AR patients and control subjects.ResultsTNF-α SNP rs1799964 and MRPL4 SNP rs11668618 were found to occur in significantly greater frequencies in the AR group compared to control group. There were no significant associations between SNPs in NF-κB, ICAM-1 and AR. The SNP-SNP interaction information analysis further indicated that there were no synergistic effects among the selected sets of polymorphisms.ConclusionsOur results suggest a strong association between AR risk and polymorphisms of MRPL4 and TNF-α genes in Han Chinese population.
Highlights
Allergic rhinitis (AR) is a chronic inflammatory disease of the nasal mucosa, which is caused by a complex interaction between genetic and environmental factors involving allergen-immunoglobulin E (IgE)-mediated stimulation of a variety of immune competent cells and release or expression of a variety of proinflammatory cytokines and mediators in allergen-sensitized individuals
Our results suggest a strong association between AR risk and polymorphisms of mitochondrial ribosomal protein L4 (MRPL4) and TNF-a genes in Han Chinese population
A more recent study by Li and colleagues has demonstrated that nasal saline irrigation as an adjunct treatment to tapered topical steroid treatment after 8 and 12 weeks in children with AR resulted in significantly decreased concentrations of sICAM-1 in nasal secretions accompanied by significant improvements in symptoms with lower concentrations of topical steroid
Summary
Allergic rhinitis (AR) is a chronic inflammatory disease of the nasal mucosa, which is caused by a complex interaction between genetic and environmental factors involving allergen-IgE-mediated stimulation of a variety of immune competent cells and release or expression of a variety of proinflammatory cytokines and mediators in allergen-sensitized individuals. We aimed to investigate associations between polymorphisms in MRPL4, NF-kB and TNF-a gene, which may influence ICAM-1 expression, and AR susceptibility in this cohort. Evidence suggests that polymorphisms in the gene coding for mitochondrial ribosomal protein L4 (MRPL4), located in close proximity to intercellular adhesion molecule-1 (ICAM-1) gene on chromosome location 19p13.2, may influence the risk factor for the development of AR
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
