Abstract
Background and objective: The high-affinity IgE receptor comprises a tetramer of the ligand-binding alpha chain, a signal-augmenting beta chain, and a signal-transducing gamma chain dimer on mast cells. We hypothesized that the three subsets of the FCER1 gene may play a role in the development of the aspirin-intolerant asthma (AIA) phenotype and analyzed these genetic polymorphisms in association with clinical parameters in AIA patients. Subjects and methods: Six polymorphisms of FCER1 (FCERIA-344C>T, FCER1A-95T>C, MS4A2-109T>C, MS4A2 E237G, FCER1G-237A>G, FCER1G-54G>T) were genotyped in 126 AIA patients compared to 177 patients with aspirin-tolerant asthma (ATA) and 222 normal health controls (NC). Results: A significant difference in the genotype frequencies of FCER1G-237A>G was detected between AIA and ATA patients (p < 0.05) both in co-dominant and recessive analysis models, whereas no significant relationships were identified between the frequencies of the other five single-nucleotide polymorphisms and AIA, ATA, and NC subjects. In addition, AIA patients carrying the homozygous AA genotype of FCER1G-237A>G exhibited significantly higher total serum IgE levels than did those with the GG/AG genotype (p = 0.012). AIA patients expressing the CT/TT genotype at FCERIA-344C>T showed a higher prevalence of serum IgE specific to Staphylococcal enterotoxin A than did those with the CC genotype (p = 0.008). Conclusion: The FCER1G-237A>G and FCERIA-344C>T polymorphisms may contribute to the development of AIA in a Korean population.
| Original language | English |
|---|---|
| Pages (from-to) | 1132-1139 |
| Number of pages | 8 |
| Journal | Respiratory Medicine |
| Volume | 102 |
| Issue number | 8 |
| DOIs | |
| Publication status | Published - 2008 Aug 1 |
| Externally published | Yes |
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Keywords
- Aspirin-intolerant asthma
- FCER1A
- FCER1G
- MS4A2
- Serum total IgE
- Specific IgE to Staphylococcal superantigen
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
Cite this
Association of three sets of high-affinity IgE receptor (FcepsilonR1) polymorphisms with aspirin-intolerant asthma. / Palikhe, Nami Shrestha; Kim, Seung Hyun; Cho, Bo Young; Ye, Young Min; Hur, Gyu Young; Park, Hae Sim.
In: Respiratory Medicine, Vol. 102, No. 8, 01.08.2008, p. 1132-1139.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Association of three sets of high-affinity IgE receptor (FcepsilonR1) polymorphisms with aspirin-intolerant asthma
AU - Palikhe, Nami Shrestha
AU - Kim, Seung Hyun
AU - Cho, Bo Young
AU - Ye, Young Min
AU - Hur, Gyu Young
AU - Park, Hae Sim
PY - 2008/8/1
Y1 - 2008/8/1
N2 - Background and objective: The high-affinity IgE receptor comprises a tetramer of the ligand-binding alpha chain, a signal-augmenting beta chain, and a signal-transducing gamma chain dimer on mast cells. We hypothesized that the three subsets of the FCER1 gene may play a role in the development of the aspirin-intolerant asthma (AIA) phenotype and analyzed these genetic polymorphisms in association with clinical parameters in AIA patients. Subjects and methods: Six polymorphisms of FCER1 (FCERIA-344C>T, FCER1A-95T>C, MS4A2-109T>C, MS4A2 E237G, FCER1G-237A>G, FCER1G-54G>T) were genotyped in 126 AIA patients compared to 177 patients with aspirin-tolerant asthma (ATA) and 222 normal health controls (NC). Results: A significant difference in the genotype frequencies of FCER1G-237A>G was detected between AIA and ATA patients (p < 0.05) both in co-dominant and recessive analysis models, whereas no significant relationships were identified between the frequencies of the other five single-nucleotide polymorphisms and AIA, ATA, and NC subjects. In addition, AIA patients carrying the homozygous AA genotype of FCER1G-237A>G exhibited significantly higher total serum IgE levels than did those with the GG/AG genotype (p = 0.012). AIA patients expressing the CT/TT genotype at FCERIA-344C>T showed a higher prevalence of serum IgE specific to Staphylococcal enterotoxin A than did those with the CC genotype (p = 0.008). Conclusion: The FCER1G-237A>G and FCERIA-344C>T polymorphisms may contribute to the development of AIA in a Korean population.
AB - Background and objective: The high-affinity IgE receptor comprises a tetramer of the ligand-binding alpha chain, a signal-augmenting beta chain, and a signal-transducing gamma chain dimer on mast cells. We hypothesized that the three subsets of the FCER1 gene may play a role in the development of the aspirin-intolerant asthma (AIA) phenotype and analyzed these genetic polymorphisms in association with clinical parameters in AIA patients. Subjects and methods: Six polymorphisms of FCER1 (FCERIA-344C>T, FCER1A-95T>C, MS4A2-109T>C, MS4A2 E237G, FCER1G-237A>G, FCER1G-54G>T) were genotyped in 126 AIA patients compared to 177 patients with aspirin-tolerant asthma (ATA) and 222 normal health controls (NC). Results: A significant difference in the genotype frequencies of FCER1G-237A>G was detected between AIA and ATA patients (p < 0.05) both in co-dominant and recessive analysis models, whereas no significant relationships were identified between the frequencies of the other five single-nucleotide polymorphisms and AIA, ATA, and NC subjects. In addition, AIA patients carrying the homozygous AA genotype of FCER1G-237A>G exhibited significantly higher total serum IgE levels than did those with the GG/AG genotype (p = 0.012). AIA patients expressing the CT/TT genotype at FCERIA-344C>T showed a higher prevalence of serum IgE specific to Staphylococcal enterotoxin A than did those with the CC genotype (p = 0.008). Conclusion: The FCER1G-237A>G and FCERIA-344C>T polymorphisms may contribute to the development of AIA in a Korean population.
KW - Aspirin-intolerant asthma
KW - FCER1A
KW - FCER1G
KW - MS4A2
KW - Serum total IgE
KW - Specific IgE to Staphylococcal superantigen
UR - http://www.scopus.com/inward/record.url?scp=47249123298&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=47249123298&partnerID=8YFLogxK
U2 - 10.1016/j.rmed.2008.03.017
DO - 10.1016/j.rmed.2008.03.017
M3 - Article
VL - 102
SP - 1132
EP - 1139
JO - Respiratory Medicine
JF - Respiratory Medicine
SN - 0954-6111
IS - 8
ER -