PMID- 23470716
OWN - NLM
STAT- MEDLINE
DCOM- 20131025
LR  - 20211021
IS  - 2092-6413 (Electronic)
IS  - 1226-3613 (Print)
IS  - 1226-3613 (Linking)
VI  - 45
IP  - 3
DP  - 2013 Mar 8
TI  - A genetic effect of IL-5 receptor alpha polymorphism in patients with 
      aspirin-exacerbated respiratory disease.
PG  - e14
LID - 10.1038/emm.2013.24 [doi]
AB  - Persistent eosinophil activation in both the upper and lower airway mucosa is a 
      central feature of aspirin-exacerbated respiratory disease (AERD). Eosinophil 
      activation and survival are profoundly influenced by interleukin 5 (IL-5) and its 
      receptor, IL-5R. In patients susceptible to allergic disorders, IL-5 receptor alpha 
      (IL5RA) polymorphisms have been reported; however, an association with AERD 
      remains unclear. We hypothesize that IL5RA polymorphisms may contribute to 
      eosinophil activation in AERD patients. We recruited 139 AERD patients, 171 
      aspirin-tolerant asthma patients and 160 normal controls. IL5RA polymorphisms 
      (-5993G>A, -5567C>G and -5091G>A) were genotyped and functional activity of 
      polymorphism was assessed by luciferase reporter assay and electrophoretic 
      mobility shift assay (EMSA). There was no significant difference in the genotype 
      frequency of the three polymorphisms among the three groups. AERD patients 
      carrying the AA genotype at -5993G>A had a significantly higher presence of 
      serum-specific immunoglobulin E (IgE) to staphylococcal enterotoxin A (P=0.008) 
      than those with the GG/GA genotype. In vitro, the -5993A allele had a higher 
      promoter activity compared with the -5993G allele in human mast cell (HMC-1; 
      P=0.030) and human promyelocytic leukemia (HL-60; P=0.013) cells. In EMSA, a 
      -5993A probe produced a specific shifted band than the -5993G had. These findings 
      suggest that a functional polymorphism in IL5RA may contribute to eosinophil and 
      mast cell activation along with specific IgE responses to staphylococcal 
      enterotoxin A in AERD patients.
FAU - Losol, Purevsuren
AU  - Losol P
AD  - Department of Allergy and Clinical Immunology, Ajou University School of 
      Medicine, Suwon, South Korea.
FAU - Kim, Seung-Hyun
AU  - Kim SH
FAU - Shin, Yoo Seob
AU  - Shin YS
FAU - Ye, Young Min
AU  - Ye YM
FAU - Park, Hae-Sim
AU  - Park HS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130308
PL  - United States
TA  - Exp Mol Med
JT  - Experimental & molecular medicine
JID - 9607880
RN  - 0 (IL5RA protein, human)
RN  - 0 (Interleukin-5 Receptor alpha Subunit)
RN  - R16CO5Y76E (Aspirin)
SB  - IM
MH  - Adult
MH  - Aspirin/*adverse effects
MH  - Electrophoretic Mobility Shift Assay
MH  - Female
MH  - Gene Frequency/genetics
MH  - Humans
MH  - Interleukin-5 Receptor alpha Subunit/*genetics
MH  - Male
MH  - Middle Aged
MH  - Phenotype
MH  - Polymorphism, Single Nucleotide/*genetics
MH  - Respiration Disorders/*chemically induced/*genetics
MH  - Transcription, Genetic
PMC - PMC3641394
EDAT- 2013/03/09 06:00
MHDA- 2013/10/26 06:00
PMCR- 2013/03/01
CRDT- 2013/03/09 06:00
PHST- 2013/03/09 06:00 [entrez]
PHST- 2013/03/09 06:00 [pubmed]
PHST- 2013/10/26 06:00 [medline]
PHST- 2013/03/01 00:00 [pmc-release]
AID - emm201324 [pii]
AID - 10.1038/emm.2013.24 [doi]
PST - epublish
SO  - Exp Mol Med. 2013 Mar 8;45(3):e14. doi: 10.1038/emm.2013.24.