机构地区:[1]哈尔滨医科大学,哈尔滨市150001 [2]黑龙江省农垦红兴隆管理局中心医院感染科,双鸭山市155811 [3]哈尔滨医科大学附属第四医院感染科,哈尔滨市150001
出 处:《中华实验和临床感染病杂志(电子版)》2018年第4期360-364,共5页Chinese Journal of Experimental and Clinical Infectious Diseases(Electronic Edition)
基 金:黑龙江省自然科学基金重点项目(No.ZD2015019)
摘 要:目的探讨肾综合征出血热(HFRS)患者急性期(包括发热期、低血压休克期、少尿期)与恢复期促炎因子和抗炎因子的变化及其作用。方法检测2016年4月至2017年6月哈尔滨医科大学第四附属医院和黑龙江省农垦红兴隆管理局中心医院收治的30例确诊为HFRS急性期和恢复期患者血清中肿瘤坏死因子-α(TNF-α)、干扰素-γ(IFN-γ)、白细胞介素-6(IL-6)和抗炎因子转化生长因子-β1(TGF-β1)、白细胞介素-10(IL-10)的水平,同期检测患者的胱抑素C(Cys-C)、肌酐(Cr)、乳酸脱氢酶(LDH)以及部分凝血活酶时间(APTT)等指标。另选同期13名健康志愿者作对照组,检测TNF-α、IFN-γ、IL-6、TGF-β1和IL-10水平。应用SAS 9.3国际标准统计学编程软件对结果进行分析。结果HFRS患者急性期IFN-γ(χ~2=4.273、P=0.0336)、TNF-α(χ~2=16.3562、P <0.0001)、IL-6(χ~2=9.752、P=0.0018)和IL-10(χ~2=6.3352、P=0.0118)水平均显著高于对照组,差异均有统计学意义。HFRS患者急性期TGF-β1水平显著低于对照组,差异有统计学意义(χ~2=7.822、P=0.0056)。HFRS患者恢复期TGF-β1水平与对照组接近或略低,差异无统计学意义(χ~2=3.000、P=0.0833)。HFRS患者发病不同时期Cys-C、Cr、LDH和APTT等指标均于急性期升高,于恢复期下降,与IFN-γ、TNF-α、IL-6和IL-10变化趋势一致。结论 HFRS急性期时IFN-γ、TNF-α和IL-6等促炎因子分泌增加,主要因CD4+CD25+Fox P3 Treg细胞(调节性T细胞)产生的抗炎因子TGF-β1分泌不足,细胞因子失衡是导致机体免疫病理损伤的重要机制。Objective To investigate the changes and effects of proinflammatory cytokines and antiinflammatory cytokines in acute phase(including febrile phase, hypotension shock phase, oliguria phase) and convalescent patients with hemorrhagic fever and renal syndrome(HFRS). Methods Levels of serum tumor necrosis factor-α(TNF-α), interferon-γ(IFN-γ), transforming growth factor-β1(TGF-β1), interleukin-6(IL-6) and interleukin-10(IL-10) in 30 patients with HFRS from the Fourth Affiliated Hospital of Harbin Medical University and Center Hopital of Heilongjiang Agricultural Reclamation Hongxinglong Administration from April 2016 to June 2017 were detected. And the levels of cystatin C, creatinine(Cr), lactate dehydrogenase(LDH), activated partial thromboplastin time(APTT) of these patients were also dectected. Thirteen healthy volunteers were selected as the control group to detect the above indexes. The results were analyzed by SAS 9.3 International Standard Statistical Programming Software. Results The levels of IFN-γ(χ^2 = 4.273, P = 0.0336), TNF-α(χ^2 = 16.3562, P〈 0.0001), IL-6(χ^2 = 9.752, P = 0.0018) and IL-10(χ^2 = 6.3352, P = 0.0118) of patient with HFRS in acute stage were all significantly higher than those of the control group, all with significant differences(all 〈P 0.05). TGF-β1 level of patients with HFRS in acute stage was significantly lower than that of the control group, with significant difference(χ^2 = 7.822, P = 0.0056). The level of TGF-β1 of patient with HFRS in recovery stage was close to or slightly lower than the control group, with no significant difference(χ^2 = 3.000, P = 0.0833). The levels of Cystatin C, Cr, LDH and APTT of patients at different HFRS stages all showed increase in the acute stage and decrease in the recovery stage, which were consistent with the trend of TNF-α, IFN-γ, IL-6 and IL-10 levels. Conclusions At acute stage of HFRS, proinflammatory cytokines such as TNF-α, IFN-γ, IL-6 increased, an
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