title: CD55 polymorphisms and risk of aspirin‑exacerbated respiratory disease.
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.
authors.affiliation: Department of Life Science, Sogang University, and Soonchunhyang University Seoul Hospital, Seoul 121-742, Republic of Korea.
authors.forename: Jin Sol
authors.initials: JS
authors.lastname: Lee
authors.forename: Joon Seol
authors.initials: JS
authors.lastname: Bae
authors.forename: Jeong-Hyun
authors.initials: JH
authors.lastname: Kim
authors.forename: Jason Yongha
authors.initials: JY
authors.lastname: Kim
authors.forename: Tae Joon
authors.initials: TJ
authors.lastname: Park
authors.forename: Charisse Flerida
authors.initials: CF
authors.lastname: Pasaje
authors.forename: Byung-Lae
authors.initials: BL
authors.lastname: Park
authors.forename: Hyun Sub
authors.initials: HS
authors.lastname: Cheong
authors.forename: Soo-Taek
authors.initials: ST
authors.lastname: Uh
authors.forename: An-Soo
authors.initials: AS
authors.lastname: Jang
authors.forename: Inseon S
authors.initials: IS
authors.lastname: Choi
authors.forename: Choon-Sik
authors.initials: CS
authors.lastname: Park
authors.forename: Hyoung Doo
authors.initials: HD
authors.lastname: Shin
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D001241:Aspirin / Q000009:adverse effects*; D055963:Asthma, Aspirin-Induced / Q000235:genetics* / Q000473:pathology; D018958:CD55 Antigens / Q000235:genetics* / Q000378:metabolism; D005541:Forced Expiratory Volume / Q000187:drug effects; D005787:Gene Frequency; D005838:Genotype; D006239:Haplotypes; D006801:Humans; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D012044:Regression Analysis; D012307:Risk Factors; D055815:Young Adult
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D018958:CD55 Antigens; D001241:Aspirin