title: Protective role of interleukin-10 promoter gene polymorphism in the pathogenesis of invasive pulmonary aspergillosis after allogeneic stem cell transplantation.
abstract: The current study attempted to evaluate the association between the IL-10 promoter gene single nucleotide polymorphism (SNP) and invasive pulmonary aspergillosis (IPA) after allogeneic stem cell transplantation (SCT) in 105 patients. Three single-nucleotide polymorphisms were investigated in the proximal region of the IL-10 promoter gene (-1082/-819/-592). Two haplotypes (1082*A/819*T/592*A [ATA] and 1082*A/819*C/592*C [ACC]) were found in the current study. The overall incidence of IPA was estimated as 14.1+/-4.5% with a median onset at 186 days post-transplant (62 approximately 405 days). An increased occurrence of IPA was noted dependent on the IL-10 haplotype (0% vs 11.5+/-6.4% vs 19.7+/-7.7% for ACC/ACC vs ATA/ACC vs ATA/ATA haplotype, P=0.0307 when comparing ACC with non-ACC haplotype). In a multivariate survival analysis using Cox's proportional hazard model, the IL-10 promoter gene SNPs were identified as an independent predictive factor for the development of IPA (P=0.012, hazard ratio (HR) 9.3), along with an histocompatibility leukocyte antigen (HLA)-identical donor (P=0.005, HR 16.3), the CD34+ cell dose transplanted (P=0.004, HR 26.5), and time-dependent chronic graft-versus-host disease (GVHD; P=0.049, HR 16.0). The IL-10 ACC haplotype was found to have an apparent protective role in the development of IPA after allogeneic transplantation, regardless of HLA-disparity or chronic GVHD.
authors.affiliation: Department of Hematology/Oncology, Kyungpook National University Hospital, Daegu, Korea.
authors.forename: K W
authors.initials: KW
authors.lastname: Seo
authors.forename: D H
authors.initials: DH
authors.lastname: Kim
authors.forename: S K
authors.initials: SK
authors.lastname: Sohn
authors.forename: N Y
authors.initials: NY
authors.lastname: Lee
authors.forename: H H
authors.initials: HH
authors.lastname: Chang
authors.forename: S W
authors.initials: SW
authors.lastname: Kim
authors.forename: S B
authors.initials: SB
authors.lastname: Jeon
authors.forename: J H
authors.initials: JH
authors.lastname: Baek
authors.forename: J G
authors.initials: JG
authors.lastname: Kim
authors.forename: J S
authors.initials: JS
authors.lastname: Suh
authors.forename: K B
authors.initials: KB
authors.lastname: Lee
mesh_terms: D000293:Adolescent; D000328:Adult; D018952:Antigens, CD34 / Q000096:biosynthesis; D001228:Aspergillosis / Q000382:microbiology* / Q000628:therapy*; D005260:Female; D006086:Graft vs Host Disease / Q000628:therapy; D006680:HLA Antigens / Q000737:chemistry; D006239:Haplotypes; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics*; D008168:Lung / Q000382:microbiology* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011110:Polymorphism, Genetic; D020641:Polymorphism, Single Nucleotide; D011401:Promoter Regions, Genetic; D016016:Proportional Hazards Models; D033581:Stem Cell Transplantation / Q000009:adverse effects*; D013997:Time Factors; D014184:Transplantation, Homologous / Q000009:adverse effects*; D016896:Treatment Outcome
chemical_list: D018952:Antigens, CD34; D006680:HLA Antigens; D016753:Interleukin-10