重症急性呼吸综合征患者血浆细胞因子水平的动态改变

目的　探讨重症急性呼吸综合征 (SARS)患者肺部严重炎症反应的发生机制。方法　选择 2 4例本院确诊的SARS患者 ,于发病第 1、第 2、第 3～ 4周及康复出院后 1个月 (发病 8～ 9周 )收集抗凝静脉血 ,以定量ELISA法检测其血浆白细胞介素 (IL) 1β、IL 2、IL 4、IL 8、IL 10、IL 12 p70、干扰素γ(IFNγ)及肿瘤坏死因子α(TNFα)水平在病程中的改变。并选择 12例正常人作为对照。结果　数据以中位数 (四分位数间距 )表示 ,与正常对照组 [IL 8:6 2 8ng/L( 3 4 3ng/L) ;TNFα :3 77ng/L( 3 4 0ng/L) ]相比 ,所有SARS病人在发病第 1周血浆IL 8浓度明显升高 [31 2 3ng/L( 78 5 1ng/L) ],P <0 0 1,75 % ( 18/2 4 )的病人在发病 3～ 4周达到最高峰 14 9 6 5ng/L( 2 4 5 97ng/L) ,P <0 0 1,至出院后 1个月 (发病 8～ 9周 )平均血浆IL 8浓度降至 8 2 3ng/L( 8 0 7ng/L)。血浆TNFα浓度也有异常升高 ,在发病第 2周为 2 3 12ng/L( 2 6 7 33ng/L) ,P <0 0 1,发病 3～ 4周达到高峰136 35ng/L( 4 76 83ng/L) ,P <0 0 5 ,出院后 1个月下降至 94 88ng/L( 2 77 18ng/L) ,仍高于正常水平 (P <0 0 1)。其他 6种细胞因子与对照组比较 ,差异无显著性。结论　SARS病人体内发生着复杂的细胞因子网络性连锁反应 ,由此产

Dynamic changes of plasma cytokine levels in patients with severe acute respiratory syndrome

OBJECTIVE: To elucidate the mechanism of strong inflammatory response in severe acute respiratory syndrome (SARS) patients. METHODS: 24 patients managed with a standard corticosteroid protocol developed by Peking Union Medical College Hospital were followed up for 2 months and their clinical outcomes were documented. Plasma levels of interleukin (IL)-1 beta, IL-2, IL-4, IL-8, IL-10, IL-12 p70, interferon gamma (IFN gamma), and tumor necrosis factor alpha (TNF alpha) were determined by quantitative ELISA during the course of disease respectively. 12 healthy blood donors were used as normal controls. RESULTS: All SARS patients had remarkably increased plasma IL-8 concentrations (median 31.23 ng/L) at the onset of disease compared with those of normal controls (6.28 ng/L, P < 0.01). Along with the course of disease IL-8 concentration kept going up and 75% (18/24) patients reached a peak median concentration of 149.65 ng/L (P < 0.01) at the third and fourth weeks. IL-8 came back to normal control levels one month after discharged from hospital. Meanwhile, SARS patients also showed high a TNF alpha level (median 23.12 ng/L) (P < 0.01) at the second week and reached a peak median of 136.35 ng/L (P < 0.05) at the third an fourth weeks. One month after discharged from hospital the plasma TNF alpha concentration fell down to a median of 94.88 ng/L, but it was still much higher than normal controls (3.77 ng/L, P < 0.01). CONCLUSION: The SARS-associated coronovirus infection may cause complex cytokine cascade. IL-8 and TNF alpha probably play important roles in mediating strong inflammatory response, which are thought to be responsible for lung injury in SARS patients.