title: Analysis of the plasma soluble human leukocyte antigen-G and interleukin-10 levels in childhood atopic asthma.
abstract: Human leukocyte antigen-G (HLA-G) has been hypothesized to be associated with the pathogenesis of asthma; however, results remain controversial. Furthermore, HLA-G expression could be modulated by the HLA-G 14-bp insertion (+)/deletion (-) polymorphism and by interleukin-10. In this study, the 14-bp polymorphism in exon 8 of the HLA-G gene, plasma soluble HLA-G, and interleukin-10 (IL-10) levels in untreated atopic asthmatic children, and in a group of age-, gender-, and ethnicity-matched normal controls were analyzed. Data showed that HLA-G 14-bp +/- polymorphism was not significant difference between the asthmatic patients and normal controls. Plasma soluble human leukocyte antigen (sHLA)-G in atopic asthma patients (n = 72; median, 179.28 U/ml) was dramatically higher compared with that of the normal controls (n = 76; median, 35.23 U/ml; p < 0.001). Receiver operating characteristic (ROC) curve analysis showed that the area under ROC curve for sHLA-G was 0.986 (p < 0.001) in atopic asthma patients versus normal controls. IL-10 levels in the asthmatic children (n = 50; median, 5.02 pg/ml) was significantly lower than that of the normal controls (n = 48; median, 12.82 pg/ml; p < 0.001). Both HLA-G 14-bp polymorphism and IL-10 levels were unrelated to plasma sHLA-G concentration in both groups. Our findings indicated that the HLA-G 14-bp polymorphism was not a risk factor, but that sHLA-G might be considered as a biomarker for the atopic asthmatic patients. Dramatically increased sHLA-G with decreased IL-10 levels may have implications in the pathogenesis of atopic asthma.
authors.affiliation: Department of Laboratory Medicine, the Second Hospital, Wenzhou Medical College, Wenzhou, Zhejiang, China.
authors.forename: Xiao-Qun
authors.initials: XQ
authors.lastname: Zheng
authors.forename: Chang-Chong
authors.initials: CC
authors.lastname: Li
authors.forename: Dan-Ping
authors.initials: DP
authors.lastname: Xu
authors.forename: Aifen
authors.initials: A
authors.lastname: Lin
authors.forename: Wei-Guang
authors.initials: WG
authors.lastname: Bao
authors.forename: Guang-Shui
authors.initials: GS
authors.lastname: Yang
authors.forename: Wei-Hua
authors.initials: WH
authors.lastname: Yan
mesh_terms: D001249:Asthma / Q000097:blood / Q000235:genetics* / Q000276:immunology* / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D002648:Child; D002675:Child, Preschool; D005260:Female; D020869:Gene Expression Profiling; D056726:Genetic Association Studies; D005838:Genotype; D006680:HLA Antigens / Q000097:blood / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I / Q000097:blood / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D006801:Humans; D016753:Interleukin-10 / Q000097:blood; D008297:Male; D010949:Plasma / Q000378:metabolism; D011110:Polymorphism, Genetic; D012307:Risk Factors
chemical_list: D015415:Biomarkers; D006680:HLA Antigens; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I; D016753:Interleukin-10