CD55 polymorphisms and risk of aspirin‑exacerbated respiratory disease

Lee,Jin  Sol; Bae, Joon  Seol; Kim,Jeong-Hyun; Kim,Jason  Yongha; Park,Tae  Joon; Pasaje,Charisse  Flerida; Park,Byung-Lae; Cheong,Hyun  Sub; Uh,Soo-Taek; Jang,An-Soo; Choi,Inseon  S.; Park,Choon-Sik; Shin,Hyoung  Doo

doi:10.3892/mmr.2012.1064

CD55 polymorphisms and risk of aspirin‑exacerbated respiratory disease

Authors:
- Jin Sol Lee
- Joon Seol Bae
- Jeong-Hyun Kim
- Jason Yongha Kim
- Tae Joon Park
- Charisse Flerida Pasaje
- Byung-Lae Park
- Hyun Sub Cheong
- Soo-Taek Uh
- An-Soo Jang
- Inseon S. Choi
- Choon-Sik Park
- Hyoung Doo Shin
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Affiliations: Department of Life Science, Sogang University, Seoul 121-742, Republic of Korea, Department of Genetic Epidemiology, SNP Genetics, Inc., Seoul 153-801, Republic of Korea, Division of Allergy and Respiratory Medicine, Soonchunhyang University Seoul Hospital, Seoul 140-743, Republic of Korea, Genome Research Center for Allergy and Respiratory Disease, Soonchunhyang University Bucheon Hospital, Bucheon 420-767, Republic of Korea, Department of Allergy, Chonnam National University Medical School and Research Institute of Medical Sciences, Gwangju 501-757, Republic of Korea
Published online on: September 5, 2012 https://doi.org/10.3892/mmr.2012.1064
Pages: 1087-1092

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Abstract

Aspirin-exacerbated respiratory disease (AERD) is a respiratory disease characterized by acute bronchial responses upon the administration of non-steroidal anti‑inflammatory drugs (NSAIDs) and the immune response by mast cells is regarded as one of the noteworthy causes of AERD pathogenesis. The complement cascade is regarded as a key mechanism for clearing pathogens from the host. CD55 is one of the proteins involved in self-recognition, a central component of the complement system and autoimmunity. To investigate the associations between CD55 single nucleotide polymorphisms (SNPs) and the risk of AERD, we carried out logistic analyses with three genetic models and further regression analysis was performed with the fall rate of forced expiratory volume in 1 sec (FEV1) by aspirin provocation. However, our results demonstrate that no CD55 polymorphisms are associated with the risk of AERD and the fall rate of FEV1 (P>0.05). Therefore, our results suggest that CD55 polymorphisms are not genetic markers of aspirin‑induced bronchospasm, including FEV1, in the population studied. Although the genetic role of CD55 has been found to be integral to human immunity, our results indicate that genetic variations of CD55 do not influence the risk of AERD and the fall rate of FEV1 in the population studied.

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