Open AccessCD55 polymorphisms and risk of aspirin-exacerbated respiratory disease
Author(s) -
Jin Sol Lee,
Joon Seol Bae,
Jeonghyun Kim,
Jason Yongha Kim,
Tae Joon Park,
Charisse Flerida A. Pasaje,
ByungLae Park,
Hyun Sub Cheong,
SooTaek Uh,
AnSoo Jang,
Inseon S. Choi,
Choon-Sik Park,
Hyoung Doo Shin
Publication year - 2012
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2012.1064
Subject(s) - immunology , population , single nucleotide polymorphism , aspirin , asthma , medicine , biology , genetics , gene , genotype , environmental health
Aspirin-exacerbated respiratory disease (AERD) is a respiratory diseasecharacterized by acute bronchial responses upon the administration of non-steroidalanti‑inflammatory drugs (NSAIDs) and the immune response by mast cells is regardedas one of the noteworthy causes of AERD pathogenesis. The complement cascade isregarded as a key mechanism for clearing pathogens from the host. CD55 is oneof the proteins involved in self-recognition, a central component of the complementsystem and autoimmunity. To investigate the associations between CD55 single nucleotidepolymorphisms (SNPs) and the risk of AERD, we carried out logistic analyses withthree genetic models and further regression analysis was performed with the fallrate of forced expiratory volume in 1 sec (FEV1) by aspirin provocation. However,our results demonstrate that no CD55 polymorphisms are associated with the riskof AERD and the fall rate of FEV1 (P>0.05). Therefore, our results suggestthat CD55 polymorphisms are not genetic markers of aspirin‑induced bronchospasm,including FEV1, in the population studied. Although the genetic role of CD55 hasbeen found to be integral to human immunity, our results indicate that geneticvariations of CD55 do not influence the risk of AERD and the fall rate of FEV1in the population studied.