TLR2 and TLR4 expression in peripheral blood mononuclear cells of patients with chronic cystic echinococcosis and its relationship with IL-10
TLR2 and TLR4 expression in peripheral blood mononuclear cells of patients with chronic cystic echinococcosis and its relationship with IL-10
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DOI：
10.1111/j.1365-3024.2011.01335.x
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发表时间：
2011-12-01
影响因子：
2.2
通讯作者：
Wen, H.
中科院分区：
文献类型：
--
作者：
Shan, J. -Y.;Ji, W. -Z.;Wen, H.
本研究旨在将 Toll 样受体 (TLR) 与慢性囊性包虫病 (CE) 患者的人类系统细胞因子联系起来。通过实时荧光定量逆转录聚合酶链反应，检测外周血单个核细胞（PBMC）中TLR2和TLR4 mRNA的表达水平，并采用ELISA法检测34例慢性CE病例（4例胆道癌患者）的细胞因子IFN-γ、IL-12p70、IL-10、IL-4和IL-17A。 泄漏； 4 名次要位置患者（其中 3 名位于肺部，1 名位于骨骼）和 22 名健康对照（HC）。 CE 组 TLR2 和 TLR4 mRNA 表达量显着升高（P < 0 05）； CE患者血清IL-10、IL-4、IL-12p70水平显着高于对照组(P < 0 05)。 CE组与HC组间IFN-γ、IL-17A水平无差异(P>0·05)。在CE患者中，TLR2表达与血清IL-10水平以及TLR4表达与血清IL-10水平呈正相关。我们的研究结果支持这样的假设：在慢性CE感染期间，TLR表达的改变可能参与细胞因子调节，这使得寄生虫能够逃避宿主免疫监视并促进慢性感染。
This study aims at relating Toll-like receptors (TLR) and human systemic cytokines in patients with chronic cystic echinococcosis (CE). By real-time fluorescent quantitative reverse-transcription polymerase chain reaction, we measured the expression level of TLR2 and TLR4 mRNA in peripheral blood mononuclear cells (PBMCs), and using ELISA, we detected the cytokines IFN-gamma, IL-12p70, IL-10, IL-4 and IL-17A from 34 chronic CE cases (four patients with biliary leakage; four patients with secondary location including three in lung and one in bone) and 22 healthy controls (HC). TLR2 and TLR4 mRNA expression were significantly higher in the CE group (P < 0 05); levels of serum IL-10, IL-4 and IL-12p70 in patients with CE were significantly higher than those in controls (P < 0 05). There were no differences in IFN-gamma and IL-17A levels between the CE group and the HC group (P > 0 05). In the patients with CE, positive correlations were noted between the expression of TLR2 and the serum level of IL-10, as well as between the expression of TLR4 and the serum level of IL-10. Our findings supported the hypothesis that during chronic CE infection, altered TLR expression might be involved in the cytokine modulation, which allowed the parasite to escape host immunosurveillance and promoted chronic infection.