摘要
目的探讨血清可溶性TNF-α、IL-1β、转化生长因子-β1(TGF-β1)、E-选择素(E-sel)和L-选择素(L-sel)在肾综合征出血热(HFRS)发病机制中的作用。方法41例HFRS患者(轻症组22例,重症组19例)纳入研究,按病期采血。分别采用放射免疫法检测TNF-α、IL-1β,ELISA法检测TGF-β1、E-sel和L-sel,自动生化仪检测肝、肾功能和PLT计数。结果从发热期至多尿期,血清IL-1β、TNF-α、E-sel和L-sel水平均升高,其峰值与对照组比较,分别为(0.56±0.10)μg/L比(0.19±0.06)μg/L、(2.41±1.61)μg/L比(0.82±0.16)μg/L、(198.4±29.2)μg/L比(56.4±25.8)μg/L、(1372.5±137.3)μg/L比(1089.9±137.9)μg/L,差异有统计学意义(P值均<0.01)。动态观察,上述细胞因子和粘附分子的变化曲线与ALT、BUN的变化趋势一致。血清TGF-β1、TGF-β1/ IL-1β和TGF-β1/TNF-α比值在病程前三期均显著降低,与PLT的变化趋势相似。结论HFRS急性期血清IL-1β、E-sel、L-sel升高和TGF-β1水平下降是造成失控性全身炎性反应和肝、肾功能损害的重要因素,在HFRS发病机制中起重要作用;合理的对症治疗和适量使用免疫调节剂可改善预后。
Objective To evaluate the role of soluble tumour necrosis factor-a(TNF-α), interleukin-1( IL- 1β), transforming growth factor-β1 (TGF-β1), E-selectin and L-selectin in the pathogenesis of hemorrhagic fever with renal syndrome (HFRS). Methods Blood samples from 41 HFRS patients (22 of mild and moderate type, 19 of severe type) were detected by radioimmunoassay for TNF-α and IL-1β, and with enzyme-linked immunosorbentassay (ELISA) for E-selectin, L-selectin and TGF-β1. Meanwhile, serum alanine aminotransferase (ALT), blood urea nitrogen (BUN) and platelet count were examined by auto-biochemical analyzer. Results During the first three stages of HFRS, serum levels of IL-1β, TNF-α, E-selectin and L-selectin were significantly increased, and their peak values were much higher than healthy control[(0.56 ± 0.10) μg/L vs (0.19 ± 0.06)μg/L, P〈 0.01, (2.41 ± 1.61) μg/L vs (0.82 ± 0. 16) μg/L, P〈0.01; (198.4 ± 29.2) μg/L vs (56.4 ±25.8) μg/L, P〈0.01; (1 372.5 ± 137.3) μg/L vs (1 089.9 ± 137.9) μg/L, P 〈 0.01] respectively. The curves of these cytokines and adhesion molecules were similar to those of ALT and BUN when observed dynamically. On the contrary, serum TGF-β1 level, TGF-β1/IL-1β ratio, TGF-β1/ TNF-α ratio and blood platelet count were significantly decreased in a parallel manner as compared with controls (P 〈 0. 05). Conclusions The increased serum levels of soluble TNF-α, IL-1β,E-selectin and L-selectin conbined with a decreased TGF-β1 level may be an important cause leading to uncontrolled systemic inflammatory response and to liver-kidney damage, and thus involved in the pathogenesis of HFRS. The combination of appropriate symptomatic therapy with immunomodulator will improve the prognosis of this disease.
出处
《中华传染病杂志》
CAS
CSCD
北大核心
2007年第8期496-499,共4页
Chinese Journal of Infectious Diseases