Positive Association between Aspirin-Intolerant Asthma and Genetic Polymorphisms of FSIP1: a Case-Case Study

BMC Pulmonary Medicine

Research Article

Inseon S Choi¹  Byung Lae Park²  Hyun Sub Cheong²  Sang Heon Cho³  Joon Seol Bae⁴  Jin Sol Lee⁴  Jeong Hyun Kim⁴  Tae Joon Park⁴  Charisse Flerida Pasaje⁴  Jason Yongha Kim⁴  Hyoung Doo Shin⁵  Soo-Taek Uh⁶  Mi-Kyeong Kim⁷  Byoung Whui Choi⁸  Choon-Sik Park⁹  Jong-Sook Park⁹  Sung-Woo Park⁹ 

[1] Department of Allergy, Chonnam National University Medical School and Research Institute of Medical Sciences, Gwangju, Republic of Korea;Department of Genetic Epidemiology, SNP Genetics, Inc., Seoul, Republic of Korea;Department of Internal Medicine and Institute of Allergy and Clinical Immunology, Seoul National University College of Medicine, Seoul, Republic of Korea;Department of Life Science, Sogang University, Seoul, Republic of Korea;Department of Life Science, Sogang University, Seoul, Republic of Korea;Department of Genetic Epidemiology, SNP Genetics, Inc., Seoul, Republic of Korea;Division of Allergy and Respiratory Medicine, Soonchunhyang University Seoul Hospital, Seoul, Republic of Korea;Division of Internal Medicine, Chungbuk National University, College of Medicine, Cheongju, Republic of Korea;Division of Pulmonology and Allergy, Department of Internal Medicine, Chung-Ang University Yongsan Hospital, Seoul, Republic of Korea;Genome Research Center for Allergy and Respiratory Disease, Soonchunhyang University Bucheon Hospital, Bucheon, Republic of Korea;

关键词: Asthma;    Aspirin;    Amino Acid Change;    Fall Rate;    Nonsynonymous SNPs;   

DOI  :  10.1186/1471-2466-10-34

 received in 2010-03-04, accepted in 2010-06-01,  发布年份 2010

来源: Springer

【 摘 要 】

BackgroundAspirin-intolerant asthma (AIA), which is caused by non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin, causes lung inflammation and reversal bronchi reduction, leading to difficulty in breathing. Aspirin is known to affect various parts inside human body, ranging from lung to spermatogenesis. FSIP1, also known as HDS10, is a recently discovered gene that encodes fibrous sheath interacting protein 1, and is regulated by amyloid beta precursor protein (APP). Recently, it has been reported that a peptide derived from APP is cleaved by α disintegrin and metalloproteinase 33 (ADAM33), which is an asthma susceptibility gene. It has also been known that the FSIP1 gene is expressed in airway epithelium.ObjectivesAim of this study is to find out whether FSIP1 polymorphisms affect the onset of AIA in Korean population, since it is known that AIA is genetically affected by various genes.MethodsWe conducted association study between 66 single nucleotide polymorphisms (SNPs) of the FSIP1 gene and AIA in total of 592 Korean subjects including 163 AIA and 429 aspirin-tolerant asthma (ATA) patients. Associations between polymorphisms of FSIP1 and AIA were analyzed with sex, smoking status, atopy, and body mass index (BMI) as covariates.ResultsInitially, 18 SNPs and 4 haplotypes showed associations with AIA. However, after correcting the data for multiple testing, only one SNP showed an association with AIA (corrected P-value = 0.03, OR = 1.63, 95% CI = 1.23-2.16), showing increased susceptibility to AIA compared with that of ATA cases. Our findings suggest that FSIP1 gene might be a susceptibility gene for aspirin intolerance in asthmatics.ConclusionAlthough our findings did not suggest that SNPs of FSIP1 had an effect on the reversibility of lung function abnormalities in AIA patients, they did show significant evidence of association between the variants in FSIP1 and AIA occurrence among asthmatics in a Korean population.

【 授权许可】

Unknown   
© Kim et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.