Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 고인송 | - |
dc.date.accessioned | 2018-01-31T07:31:56Z | - |
dc.date.available | 2018-01-31T07:31:56Z | - |
dc.date.issued | 2011-02 | - |
dc.identifier.citation | International Archives of Allergy and Immunology, 2011, 155(4), P.395-402 | en_US |
dc.identifier.issn | 1018-2438 | - |
dc.identifier.uri | https://www.karger.com/Article/FullText/321267 | - |
dc.description.abstract | Background: Aspirin-intolerant asthma (AIA) is a clinical syndrome characterized by acute bronchoconstriction following the ingestion of aspirin. Solute carrier family 22, member 2 (SLC22A2), also known as organic cation transporter 2 (OCT2), is predominantly expressed in the luminal membrane of airway epithelial cells and has been shown to mediate the transport of prostaglandins on the cyclooxygenase pathway which is regulated by aspirin blockage. Recently, SLC22A2-mediated uptake inhibition by several nonsteroidal anti-inflammatory drugs and decreased SLC22A2 transport activity by its genetic variants have been elucidated in asthma. Methods: To investigate the associations between AIA and genetic polymorphisms of the SLC22A2 gene, 18 variants were genotyped in 163 AIA subjects and 429 aspirin-tolerant asthma (ATA) controls. Logistic analyses were used to evaluate p values for the associations of SLC22A2 polymorphisms with AIA. Results: One common polymorphism in intron 5, i.e. rs316021, was significantly associated with susceptibility to AIA (p = 0.004, P(corr) = 0.05, OR = 0.60, 95% Cl = 0.43-0.85 in a codominant model). The minor allele frequency of rs316021 in the AIA group was significantly lower than that in the ATA controls. In addition, a polymorphism in intron 4 (rs3912161) and a haplotype (SLC22A2-ht3) showed significantly stronger association signals with the FEV(1) fall rate induced by aspirin provocation in AIA subjects compared with ATA controls (p = 0.004, P(corr) = 0.05). Conclusion: Our findings suggest that SLC22A2 could be a susceptibility gene for aspirin intolerance in asthmatics. | en_US |
dc.description.sponsorship | This work was supported by a grant from the Korea Health 21 R&D Project (A010249); grant number M1-0302-00-0073 from the Korea Science and Engineering Foundation (KOSEF) funded by the Korean government (MEST) (No. 2009-0080157); an Intramural Research Grant from the Korea National Institute of Health (No. 4800-4845-300-260-00); an Intramural Research Grant from Sogang University (No. 200810021.01), and a Priority Research Centers Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science, and Technology (2009-0093822). | en_US |
dc.language.iso | en | en_US |
dc.publisher | KARGER | en_US |
dc.subject | Solute carrier family 22, member 2 | en_US |
dc.subject | Aspirin-intolerant asthma | en_US |
dc.subject | Polymorphism | en_US |
dc.subject | Haplotype | en_US |
dc.title | Possible Association of SLC22A2 Polymorphisms with Aspirin-Intolerant Asthma | en_US |
dc.type | Article | en_US |
dc.relation.no | 4 | - |
dc.relation.volume | 155 | - |
dc.identifier.doi | 10.1159/000321267 | - |
dc.relation.page | 395-402 | - |
dc.relation.journal | INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY | - |
dc.contributor.googleauthor | Park, Tae-Joon | - |
dc.contributor.googleauthor | Kim, Jeong-Hyun | - |
dc.contributor.googleauthor | Bae, Joon-Seol | - |
dc.contributor.googleauthor | Chun, Ji-Yong | - |
dc.contributor.googleauthor | Lee, Jin-Sol | - |
dc.contributor.googleauthor | Kim, Jason Yongha | - |
dc.contributor.googleauthor | Pasaje, Charisse Flerida | - |
dc.contributor.googleauthor | Park, Byung-Lae | - |
dc.contributor.googleauthor | Cheong, Hyun Sub | - |
dc.contributor.googleauthor | Koh, In Song | - |
dc.relation.code | 2011204091 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | insong | - |
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