Association of Eotaxin gene family with asthma and serum total IgE

Hyoung Doo Shin, Lyoung Hyo Kim, Byung Lae Park, Ji Hyun Jung, Jun Yeon Kim, Il Yup Chung, Jung Sun Kim, June Hyuk Lee, Sun Hee Chung, Yong Hoon Kim, Hae Sim Park, Jeong Hee Choi, Young Mok Lee, Sung Woo Park, Byoung Whui Choi, Soo Jong Hong, Choon Sik Park

Research output: Contribution to journalArticlepeer-review

41 Scopus citations

Abstract

The Eotaxin gene family (Eotaxin1, Eotaxin2 and Eotaxin3) recruits and activates CCR3-bearing cells such as eosinophils, mast cells and Th2 lymphocytes that play a major role in allergic disorders. To date, the effect of polymorphisms of Eotaxin genes on asthma phenotypes has not been thoroughly examined. In our research, we sequenced whole regions of the Eotaxin gene family to identify polymorphisms, which may be involved in the development of asthma and total serum IgE. We have identified 37 SNPs in the Exotaxin gene family (Exotaxin1, 2 and 3), and 17 common polymorphic sites were selected for genotyping in our asthma cohort (n=721). Statistical analysis revealed that the EOT2+1265A>G G* allele showed significantly lower frequency in asthmatics than in normal healthy controls (0.14 versus 0.23, P=0.002), and that distribution of the EOT2+1265A>G G* allele-containing genotypes was also much lower in asthmatics (26.3 versus 40.8%, P=0.003). In addition, a non-synonymous SNP in Eotaxin1, EOT1+123AIa>Thr showed significant association with total serum IgE levels (P=0.002-0.02). The effect of EOT1+123AIa> Thr on total serum IgE appeared in a gene-dose-dependent manner. Our findings suggest that the development of asthma may be associated with EOT2+1265A>G polymorphisms, and the susceptibility to high IgE production may be attributed to the EOT1+ 123AIa> Thr polymorphism. Eotaxin variation/haplotype information identified in this study might provide valuable insights into strategies for the control of asthma.

Original languageEnglish (US)
Pages (from-to)1279-1285
Number of pages7
JournalHuman molecular genetics
Volume12
Issue number11
DOIs
StatePublished - Jun 1 2003
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Genetics(clinical)

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