A single nucleotide polymorphism on the promoter of eotaxin1 associates with its mRNA expression and asthma phenotypes
- Authors
- Chang, HunSoo; Kim, Jung Sun; Lee, JuneHyuk; Cho,JungIl; Rhim,TaiYoun; Uh, Soo-Taek; Park, Byung Lae; Chung, Il Yup; Park, Choon-Sik; Shin, Hyoung Doo
- Issue Date
- Feb-2005
- Publisher
- American Association of Immunologists
- Citation
- Journal of Immunology, v.174, no.3, pp.1525 - 1531
- Indexed
- SCIE
SCOPUS
- Journal Title
- Journal of Immunology
- Volume
- 174
- Number
- 3
- Start Page
- 1525
- End Page
- 1531
- URI
- https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/46088
- DOI
- 10.4049/jimmunol.174.3.1525
- ISSN
- 0022-1767
- Abstract
- Eotaxin1 plays a pivotal role in eosinophil-associated inflammation. Previously, we demonstrated 14 single-nucleotide polymorphisms (SNPs) in the human eotaxin 1 gene and the association between the EOT+67G>A allele and the level of IgE,. In this study. we investigated the association between the SNPs and plasma eotaxin 1 levels. peripheral blood eosinophil counts, and PC20 methacholine values in normal and asthmatic subjects, and the effects of SNI's on the process of eotaxin 1 production. The EOT-576C>T and EOT-384A>G polymorphisms and haplotypes (ht1 and ht4) were si--nificantly associated with pin a eotaxin 1 levels in the asthmatics (p < 0.001-0.040). The log [plasma eotaxin1] values correlated with the log (serum total 1g] values in the asthmatics and the normal controls (p = 0.012 and p = 0.004, respectively), and with the log [PC20 methacholine] values in the asthmatics (p = 0.014). A DNA-protein complex was formed with EOT-384A > G. but not with the other SNTs or the promoter. The interaction was stronger with the minor allele than with the common allele. and was reduced upon TNT-alpha exposurte. TNF-alpha-stimulated PBMCs front the asthmatics with the minor allele homozygote expressed sigificantly lower levels of eotaxin 1 mRNA than those front individuals with the common allele. The EOT+67G>A polymorphism. which substitutes alanine with threonine, did not affect eotaxin1 production or activity. Our data suggest that the EOT-384.A>G SNP participates in the regulation of eotaxinl expression by providing a potential binding site for a repressor. and that the ANOVA of EOT-3844 > G may predict asthma phenotypes.
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