62 453

Cited 14 times in

Association of the CCR3 gene polymorphism with aspirin exacerbated respiratory disease.

DC Field Value Language
dc.contributor.authorKim, SH-
dc.contributor.authorYang, EM-
dc.contributor.authorLee, HN-
dc.contributor.authorChoi, GS-
dc.contributor.authorYe, YM-
dc.contributor.authorPark, HS-
dc.date.accessioned2011-05-17T02:14:30Z-
dc.date.available2011-05-17T02:14:30Z-
dc.date.issued2010-
dc.identifier.issn0954-6111-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/2627-
dc.description.abstractINTRODUCTION: Aspirin hypersensitivity represents two distinct clinical syndromes, such as aspirin exacerbated respiratory disease (AERD) and aspirin-intolerant chronic urticaria/angioedema (AICU) which have different clinical phenotypes resulting from different genetic backgrounds in a Korean population. Persistent eosinophilic inflammation in airway is a characteristic feature of AERD and chemokine CC motif receptor 3 (CCR3) plays an important role in eosinophilic infiltration into the asthmatic airway.



OBJECTIVES: The main objective of this study is to investigate the association between CCR3 gene polymorphisms and aspirin hypersensitivity, including AERD and AICU.



METHODS: CCR3 mRNA expression was measured after an aspirin provocation test by real-time PCR. In total, 330 patients with aspirin hypersensitivity (191 AERD and 139 AICU) and 217 normal healthy controls (NC) were genotyped for two CCR3 promoter polymorphisms (-520T/G and -174C/T), and the functional effects of the polymorphisms were analyzed applying a luciferase reporter assay and an electrophoretic mobility shift assay.



RESULTS: CCR3 mRNA expression was significantly increased after aspirin provocation in AERD patients (P=0.002) but not in AICU patients. An in vitro functional study showed that the reporter construct having a -520G allele exhibited significantly higher promoter activity compared with the construct having a -520T allele in human myeloid (U937), lymphoid (Jurkat), and mast (HMC-1) cell lines (P<0.001). We found -520G and -174T specific bands on EMSA.



CONCLUSION: This result suggests that the CCR3 genetic polymorphisms may contribute to the development of the AERD phenotype and may be used as a genetic marker for differentiating between the two major aspirin hypersensitivity phenotypes.
-
dc.language.isoen-
dc.subject.MESHAdult-
dc.subject.MESHAspirin/adverse effects/*immunology-
dc.subject.MESHCase-Control Studies-
dc.subject.MESHDrug Hypersensitivity/*genetics/immunology-
dc.subject.MESHFemale-
dc.subject.MESHGene Frequency/genetics/immunology-
dc.subject.MESHGenetic Markers-
dc.subject.MESHGenotype-
dc.subject.MESHHumans-
dc.subject.MESHMale-
dc.subject.MESHPhenotype-
dc.subject.MESH*Polymorphism, Genetic-
dc.subject.MESHReceptors, CCR3/*genetics-
dc.subject.MESHRespiration Disorders/chemically induced/*genetics/immunology-
dc.subject.MESHUrticaria/chemically induced/*genetics/immunology-
dc.titleAssociation of the CCR3 gene polymorphism with aspirin exacerbated respiratory disease.-
dc.typeArticle-
dc.identifier.pmid20022477-
dc.identifier.urlhttp://linkinghub.elsevier.com/retrieve/pii/S0954-6111(09)00388-6-
dc.contributor.affiliatedAuthor김, 승현-
dc.contributor.affiliatedAuthor최, 길순-
dc.contributor.affiliatedAuthor예, 영민-
dc.contributor.affiliatedAuthor박, 해심-
dc.type.localJournal Papers-
dc.identifier.doi10.1016/j.rmed.2009.11.024-
dc.citation.titleRespiratory medicine-
dc.citation.volume104-
dc.citation.number5-
dc.citation.date2010-
dc.citation.startPage626-
dc.citation.endPage632-
dc.identifier.bibliographicCitationRespiratory medicine, 104(5):626-632, 2010-
dc.identifier.eissn1532-3064-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Allergy
Journal Papers > Research Organization > Regional Clinical Trial Center

qrcode

해당 아이템을 이메일로 공유하기 원하시면 인증을 거치시기 바랍니다.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse