脓毒症急性肺损伤患者外周血Th22和Th17细胞水平变化及临床意义
详细信息    查看全文 | 推荐本文 |
  • 英文篇名:Changes and significance of peripheral blood Th22 and Th17 cells in sepsis patients with acute lung injury
  • 作者:邓欣雨 ; 赵燕 ; 罗成玲 ; 何婧
  • 英文作者:DENG Xin-yu;ZHAO Yan;LUO Cheng-ling;HE Jing;Second Affiliated Hospital of Chongqing Medical University;
  • 关键词:Th22细胞 ; Th17细胞 ; 脓毒症 ; 急性肺损伤 ; 白细胞介素-22
  • 英文关键词:Th22 cells;;Th17 cells;;Sepsis;;Acute lung injury;;Interleukin-22
  • 中文刊名:ZHYY
  • 英文刊名:Chinese Journal of Nosocomiology
  • 机构:重庆医科大学附属第二医院呼吸与危重症医学科;重庆医科大学附属第三医院(捷尔医院)呼吸疾病中心;
  • 出版日期:2019-02-09 07:00
  • 出版单位:中华医院感染学杂志
  • 年:2019
  • 期:v.29
  • 基金:国家自然科学基金资助项目(81600060)
  • 语种:中文;
  • 页:ZHYY201904005
  • 页数:5
  • CN:04
  • ISSN:11-3456/R
  • 分类号:26-30
摘要
目的探讨外周血Th22和Th17细胞在脓毒症急性肺损伤患者中的水平变化及其临床意义。方法选取2013年1月-2017年1月于医院就诊的脓毒症患者320例为研究对象,根据是否存在急性肺损伤,将其分为脓毒症普通组252例和脓毒症急性肺损伤组68例。检测两组患者外周血Th22和Th17细胞水平与外周血白细胞介素22(IL-22)、IL-6和IL-17的浓度。采用受试者工作特征曲线(ROC)评估外周血Th22和Th17细胞对脓毒症急性肺损伤早期诊断的效能。结果脓毒症急性肺损伤组肺损伤预测(LIPS)评分、IL-6、IL-17、IL-22、Th17及Th22细胞分别为(8.73±0.18)分、13.02(11.55,14.87)ng/L、22.06(18.42,25.89)ng/L、22.10(19.75,25.04)ng/L、(8.30±1.28)%及(6.40±0.93)%高于脓毒症普通组(P<0.05)。LIPS评分、IL-17、IL-22、Th17细胞及Th22细胞是脓毒症患者发生脓毒症急性肺损伤的影响因素(P<0.05)。相关性分析显示,脓毒症急性肺损伤患者外周血Th22细胞比例与LIPS评分、IL-22及Th17细胞比例呈正相关(P<0.05);同时外周血Th17细胞比例与LIPS评分及IL-17呈正相关(P=0.006)。外周血Th22细胞曲线下面积为0.837(0.768~0.901),其截断值为6.21%时,其早期诊断脓毒症急性肺损伤的敏感性和特异性分别73.72%和88.13%,优于外周血Th17细胞,但差异无统计学意义(P=0.397)。结论外周血Th22和Th17细胞在脓毒症急性肺损伤患者中明显升高,对于脓毒症急性肺损伤的早期诊断,具有重要的临床价值。
        OBJCETIVE To investigate the change and clinical significance of peripheral blood Th22 and Th17 cells in sepsis patients with acute lung injury.METHODS A total of 320 patients with sepsis treated in our hospital from Jan.2013 to Jan.2017 were enrolled in the study,and divided into normal sepsis group(252 cases)and sepsis with acute lung injury group(68 cases)according to whether complicated with acute lung injury.The levels of Th22 and Th17 cells in peripheral blood were detected by flow cytometry.The levels of interleukin 22(IL-22)and interleukin 17(IL-17)in peripheral blood were detected by enzyme-linked immunosorbent assay.The efficacy of Th22 and Th17 cells in peripheral blood in the early diagnosis of sepsis with acute lung injury was evaluated by the receiver operating characteristic curve(ROC).RESULTS The Lung Injury Prediction Score(LIPS),interleukin(IL-6),IL-17,IL-22,Th17 and Th22 cells in peripheral blood of the patients in the sepsis with acute lung injury group were(8.73±0.18)points,13.02(11.55,14.87)ng/L,22.06(18.42,25.89)ng/L,22.10(19.75,25.04)ng/L,(8.30±1.28)% and(6.40±0.93),which were significantly higher than those in normal sepsis controls(P<0.05).The LIPS score,IL-17,IL-22,Th17 and Th22 cells ratio were independent risk factors for sepsis with acute lung injury(P<0.05).The correlation analysis showed that there were significant positive correlations among the ratio of Th22 cells in peripheral blood and LIPS score,IL-22 and Th17 cells in sepsis patients with acute lung injury.Meanwhile,the ratio of Th17 cells was positively correlated with LIPS score(P=0.006).The area under the curve was 0.837(0.768~0.901),and when the cut-off value of peripheral blood Th22 cells was 6.21%,the sensitivity and specificity of early diagnosis of sepsis with acute lung injury were 73.72%and 88.13%,respectively,which were better than those of Th17 cells.However,the difference was not significant(P=0.397).CONCLUSIONThe Th22 and Th17 cells levels in peripheral blood are significantly increased in sepsis patients with acute lung injury patients,which has important clinical value for early diagnosis of sepsis with acute lung injury.
引文
[1] Kida Y,Ohshimo S,Shime N.Optimal cutoff value for lung injury prediction score and potential confounders for identifying the risk of developing acute respiratory distress syndrome[J].Crit Care Med,2017,45(6):e624-e625.
    [2] Tang L,Bai J,Chung CS,et al.Active players in resolution of shock/sepsis induced indirect lung injury:immunomodulatory effects of Tregs and PD-1[J].J Leukoc Biol,2014,96(5):809-820.
    [3] Perusina Lanfranca M,Lin Y,Fang J,et al.Biological and pathological activities of interleukin-22[J].J Mol Med(Berl),2016,94(5):523-534.
    [4]顾丽萍,杨贵丽,陈幼发,等.Th22细胞及其功能分子IL-22在狼疮性肾炎中的作用研究[J].中国免疫学杂志,2017,33(5):755-758.
    [5] Li J,Li M,Su L,et al.Alterations of T helper lymphocyte subpopulations in sepsis,severe sepsis,and septic shock:a prospective observational study[J].Inflammation,2015,38(3):995-1002.
    [6] Dellinger RP,Levy MM,Rhodes A,et al.Surviving sepsis campaign:international guidelines for management of severe sepsis and septic shock:2012[J].Intensive Care Med,2013,39(2):165-228.
    [7] Kalbitz M,Karbach M,Braumueller S,et al.Role of complement C5in experimental blunt chest trauma-induced septic acute lung injury(ALI)[J].PLoS One,2016,11(7):e0159417.
    [8]雷波,玄秀云,樊卫平,等.Th22细胞分泌IL-22激活STAT3通路促进人卵巢癌发展[J].免疫学杂志,2018,34(6):492-498.
    [9]林洁,胡志宏,王洁,等.Th22细胞在肠道病毒71型感染导致手足口病患儿中的表达及其临床意义[J].中华临床感染病杂志,2017,10(2):146-149.
    [10] Liu T,Peng L,Yu P,et al.Increased circulating Th22and Th17cells are associated with tumor progression and patient survival in human gastric cancer[J].J Clin Immunol,2012,32(6):1332-1339.
    [11] de Lima Silveira E,de Sousa JR,de Sousa Aarao TL,et al.New immunologic pathways in the pathogenesis of leprosy:role for Th22cytokines in the polar forms of the disease[J].J Am Acad Dermatol,2015,72(4):729-730.
    [12] Guo J,Tao W,Tang D,et al.Th17/regulatory T cell imbalance in sepsis patients with multiple organ dysfunction syndrome:attenuated by high-volume hemofiltration[J].Int J Artif Organs,2017,40(11):607-614.
    [13] Khare V,Paul G,Movadat O,et al.IL10R2overexpression promotes IL22/STAT3signaling in colorectal carcinogenesis[J].Cancer Immunol Res,2015,3(11):1227-1235.
    [14] Jie Z,Liang Y,Yi P,et al.Retinoic acid regulates immune responses by promoting IL-22and modulating S100proteins in viral hepatitis[J].J Immunol,2017,198(9):3448-3460.
    [15]顾延会,符丹丹,饶习敏,等.树突状细胞在慢性阻塞性肺疾病急性发作期患者感染中对T细胞的调控作用[J].中华医院感染学杂志,2016,26(16):3682-3684.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700