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    刘雅婷, 刘健胜, 卢思广, 于艳辉, 苗莉. 呼吸道前驱感染对IgA血管炎患儿血清IL-23、MIP-3α水平的影响及意义[J]. 徐州医科大学学报, 2017, 37(7): 478-482.
    引用本文: 刘雅婷, 刘健胜, 卢思广, 于艳辉, 苗莉. 呼吸道前驱感染对IgA血管炎患儿血清IL-23、MIP-3α水平的影响及意义[J]. 徐州医科大学学报, 2017, 37(7): 478-482.
    LIU Yating, LIU Jiansheng, LU Siguang, YU Yanhui, MIAO Li. Changes of serum IL-23 and MIP-3α levels in children with IgA vasculitis after respiratory tract infection and their significance[J]. Journal of Xuzhou Medical University, 2017, 37(7): 478-482.
    Citation: LIU Yating, LIU Jiansheng, LU Siguang, YU Yanhui, MIAO Li. Changes of serum IL-23 and MIP-3α levels in children with IgA vasculitis after respiratory tract infection and their significance[J]. Journal of Xuzhou Medical University, 2017, 37(7): 478-482.

    呼吸道前驱感染对IgA血管炎患儿血清IL-23、MIP-3α水平的影响及意义

    Changes of serum IL-23 and MIP-3α levels in children with IgA vasculitis after respiratory tract infection and their significance

    • 摘要: 目的探讨呼吸道前驱感染对IgA血管炎(IgAV)患儿血清白细胞介素-23(IL-23)和巨噬细胞炎性蛋白-3α(MIP-3α)水平的影响及意义。方法收集急性期IgAV患儿共47例,根据有无呼吸道前驱感染,将其分为无呼吸道感染的IgAV组(IgAV1组)、有呼吸道感染的IgAV组(IgAV2组),并收集同期呼吸道感染组23例、正常对照组20例,所有受试者共90例。第一步运用抗体芯片半定量检测各组中的部分受试者(总例数=16)血清细胞因子水平,采用倍数分析方法筛选出可能有意义的生物因子,再进一步用酶联免疫吸附试验(ELISA)定量检测各组中其余受试者(总例数=74)血清该细胞因子的水平。结果①运用抗体芯片半定量检测和分析,初步筛选出IL-23和MIP-3α可能为有意义的细胞因子。②运用ELISA定量检测血清IL-23、MIP-3α水平发现:IgAV患儿血清IL-23的水平〔(48.56±34.27)ng/L〕与正常对照组〔(5.85±3.69)ng/L〕相比明显升高,差异有统计学意义(P<0.01)。IgAV1组、IgAV2组、呼吸道感染组血清IL-23水平均明显高于正常对照组,IgAV2组血清IL-23水平高于其余各组,差异均有统计学意义(P<0.05)。IgAV1组、IgAV2组的血清MIP-3α水平与正常对照组相比,差异无统计学意义(P>0.05)。结论MIP-3α与IgAV的发病无明显相关。异常升高的IL-23水平可能参与IgAV的免疫发病机制。呼吸道感染可能通过促使IgAV患儿血清IL-23水平升高,进而引起免疫紊乱,诱发IgAV。

       

      Abstract: Objective To explore the changes and significance of serum interleukin-23 (IL-23) and macrophage inflammatory protein-3α (MIP-3α) levels in children with IgA vasculitis (IgAV) after respiratory tract infection. MethodsA total of 47 patients with acute IgAV were divided into two groups: Group IgAV1 without respiratory tract infection and Group IgAV2 with respiratory tract infection. Meanwhile, another 23 patients with respiratory tract infection and 20 healthy controls were enrolled into the study. There were 90 patients in total. The levels of serum cytokines were semi-quantitatively detected by antibody array (n=16). Potential biomarkers were screened out. Furthermore, the levels of serum IL-23 and MIP-3α were measured by enzyme-linked immunosorbent assay (ELISA) (n=74). ResultsIL-23 and MIP-3α were screened out as potential biomarkers. The level of serum IL-23 in children with IgAV [(48.56±34.27) ng/L] was significantly higher than that in normal control group [ (5.85±3.69) ng/L] (P<0.01). The levels of serum IL-23 in Groups IgAV1, IgAV2 and the respiratory tract infection group were significantly elevated, compared with the normal control group (P<0.05). Group IgAV2 presented a substantially higher level of IL-23 than Group IgAV1 and the respiratory tract infection group (P<0.05). There was no significant difference in serum MIP-3α level between Groups IgAV1 and IgAV2 and the normal control group (P>0.05). ConclusionsMIP-3α is not associated with the pathogenesis of IgAV. Abnormally elevated serum IL-23 levels may be involved in the immunopathogenesisof IgAV. Respiratory tract infection may contribute to elevated serum IL-23 levels and cause immunological disorder which then induces IgAV.

       

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