期刊文献+

维生素D通过JAK/STAT信号通路影响毛细支气管炎患儿免疫应答的研究 被引量:8

Effect of Vitamin D on immune response of children with bronchiolitis through JAK/STAT signaling pathway
下载PDF
导出
摘要 目的探讨维生素D用于毛细支气管炎患儿的治疗效果及如何通过对JAK/STAT信号通路影响患儿机体的免疫应答。方法选取96例住院毛细支气管炎患儿,按随机数表法分为观察组和对照组,各48例。对照组采取常规治疗,观察组在对照组基础上联合维生素D,两组疗程均3~7 d。比较两组患儿的憋喘消失时间、肺部哮鸣音消失时间、呼吸困难消失时间、住院时间、入院时和治疗后的血清IgA、IgG、IgM及IgE水平以及外周血单个核细胞(PBMCs)中STAT1、STAT2、IRF9表达。结果观察组各项症状缓解时间均显著短于对照组,差异有统计学意义(P<0.05)。治疗后,对照组血清IgA、IgG、IgM、IgE水平较治疗前无明显变化(P>0.05)。观察组治疗后的血清IgA、IgG分别为(0.41±0.11)g/L、(7.34±1.87)g/L,较治疗前明显升高且高于同期对照组;IgE为(118.74±23.63)×10^(3) IU/L,较治疗前明显降低且低于同期对照组,差异均有统计学意义(P<0.05)。治疗后,对照组PBMCs中STAT1、STAT2、IRF9表达较治疗前无明显变化(P>0.05)。观察组治疗后的PBMCs中STAT1、STAT2、IRF9表达量分别为(0.57±0.17)、(0.63±0.18)、(0.47±0.15),均较治疗前明显上调,且高于同期对照组,差异均有统计学意义(P<0.05)。结论维生素D可激活毛细支气管炎患儿PBMCs中JAK-STAT信号转导途径,促进STAT1、STAT2、IRF-9等特异性分子表达的上调,加强机体的免疫应答,促进患儿病情好转。 Objective To explore the therapeutic effect of vitamin D in children with bronchiolitis and how to affect the immune response of children with JAK/STAT signaling pathway.Methods A total of 96 patients with bronchiolitis hospitalized from April 2017 to November 2019 were selected and divided into the observation group and the control group according to random number table method,48 cases in each group.The control group received conventional treatment,and the observation group combined with vitamin D on the basis of the control group.The treatment course of both groups was 3~7 days.The time of breathlessness disappear,wheezing in the lungs disappear,dyspnea disappear,hospital stay,the levels of serum IgA,IgG,IgM,and IgE and the peripheral blood mononuclear cells(PBMCs)expression of STAT1,STAT2 and IRF9 on admission and after treatment were compared between the two groups.Results The remission time of each symptom in the observation group was significantly shorter than that in the control group(P<0.05).After treatment,the levels of serum IgA,IgG,IgM,and IgE in the control group had no significant changes compared with before treatment(P>0.05).The serum IgA and IgG of the observation group after treatment were(0.41±0.11)g/L and(7.34±1.87)g/L,which were significantly higher than before treatment and higher than the control group during the same period.The level of IgE was(118.74±23.63)×10^(3) IU/L,which was significantly lower than before treatment and that of the control group during the same period(P<0.05).After treatment,the expression of STAT1,STAT2,and IRF9 in PBMCs of the control group had no significant change compared with that before treatment(P>0.05).The expression levels of STAT1,STAT2,and IRF9 in PBMCs after treatment in the observation group were(0.57±0.17),(0.63±0.18),and(0.47±0.15),which were significantly higher than before treatment and the control group during the same period(P<0.05).Conclusion Vitamin D can activate the JAK-STAT signal transduction pathway in PBMCs of children with bronchioli
作者 唐川婷 冯琴 TANG Chuan-ting;FENG Qin(Department of Pediatrics,West China Guang'an Hospital of Sichuan University,Guang'an,Sichuan 638000,China)
出处 《临床肺科杂志》 2021年第8期1184-1188,共5页 Journal of Clinical Pulmonary Medicine
关键词 毛细支气管炎 维生素D 酪氨酸蛋白激酶信号转录与转录激活因子 免疫应答 bronchiolitis Vitamin D Janus kinase-signal transducers and activators of transcription immune response
  • 相关文献

参考文献14

二级参考文献143

  • 1Ghoreschi K, Laurence A, O'Shea JJ. Janus kinases in immune cell signaling [J]. Immunol Rev, 2009, 228 (1): 273-287. 被引量:1
  • 2Schindler C, Levy DE, Decker T. JAK-STAT signaling: fi'om interferons to cytokines [J]. J Biol Chem, 2007, 282 (28): 20059-20063. 被引量:1
  • 3Kershaw NJ, Murphy JM, Lucet IS, et al. Regulation of Janus kinases by SOCS proteins [J]. Biochem Soe Trans, 2013, 41 (4): 1042-1047. 被引量:1
  • 4Sasaki A, Yasukawa H, Suzuki A, et al. Cytokine-inducible SH2 protein-3 (CIS3/SOCS3) inhibits Janus tyrosine kinase by binding through the N-terminal kinase inhibitory region as well as SH2 domain[J]. Genes Cells, 1999, 4(6): 339-351. 被引量:1
  • 5Babon JJ, Kershaw NJ, Murphy JM, et al. Suppression of cytokine signaling by SOCS3: characterization of the mode of inhibition and the basis of its specificity [J]. Immunity, 2012, 36 (2): 239-250. 被引量:1
  • 6Kershaw NJ, Murphy JM, Lian NP, et al. SOCS3 binds specific receptor-JAK complexes to control cytokine signaling by direct kinase inhibition [J]. Nature structural & molecular biology, 2013, 20 (4): 469-476. 被引量:1
  • 7Trengove MC, Ward AC. SOCS proteins in development and disease [J]. Am J Clin Exp Immunol, 2013, 2 (1): 1-29. 被引量:1
  • 8Gil AP, Kostopoulou E, Karageorgou I, et al. Increased growth hormone receptor (GHR) degradation due to over-expression of cytokine inducible SH2 domain-containing protein (CIS) as a cause of GH transduction defect (GHTD) [J]. J Pediatr Endoerinol Metab, 2012, 25 (9-10): 897-908. 被引量:1
  • 9Peng Y, Lee J, Zhu C, et al. A novel role for protein inhibitor of activated STAT (PIAS) proteins in modulating the activity of Zimp7, a novel PIAS-like protein, in androgen receptor-mediated transcription [J]. J Biol Chem, 2010, 285 (15): 11465-11475. 被引量:1
  • 10Quintas-Cardama A, Verstovsek S. Molecular pathways: Jak/STAT pathway: mutations, inhibitors, and resistance [J]. Clin Cancer Res, 2013, 19 (8): 1933-1940. 被引量:1

共引文献340

同被引文献95

引证文献8

二级引证文献19

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部