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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Effect of bacterial endotoxin LPS on expression of INF-gamma and IL-5 in T-lymphocytes from asthmatics.
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Effect of bacterial endotoxin LPS on expression of INF-gamma and IL-5 in T-lymphocytes from asthmatics.

机译：细菌内毒素LPS对哮喘患者T淋巴细胞中INF-γ和IL-5表达的影响。

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Epidemiological evidence, in vitro studies and animal models suggest that exposure to the bacterial endotoxin lipopolysaccharide (LPS) can influence the development and severity of asthma. Although it is known that signaling through Toll-like receptors (TLR) is required for adaptive T helper cell type 1 and 2 responses, it is unclear whether the LPS ligand TLR 4 is expressed on CD4(+) and CD8(+) T-lymphocytes and if so, whether LPS could modulate the T(H)1 or T(H)2 response in this context. The present authors have, therefore, examined the expression of TLR 4 on peripheral blood CD4(+) and CD8(+) T-lymphocytes using RT-PCR method and FACS analyses. Furthermore, the authors have studied the IL-12-induced expression of the T(H)1-associated cytokine INF-gamma and the IL-4-induced expression of the T(H)2-specific cytokine IL-5 in the presence of LPS using ELISA and compared nine atopic asthmatic subjects and eleven nonatopic normal volunteers. There was an increased anti-CD3/anti-CD28-induced IL-5 expression in T cells of asthmatics compared with normals (p<0.01). In the presence of IL-4 (10 ng/ml), there was an additional increase in IL-5 expression and this additional increase was greater in T cells of normals compared with asthmatics (p<0.05). There was an expression of INF-gamma in anti-CD3/anti-CD28-induced T-lymphocytes without differences between both groups (NS). In the presence of IL-12 (10 ng/ml), there was an increase in INF-gamma release without differences between normals and asthmatics (NS). In the presence of different concentrations of LPS (10 ng/ml, 1 mug/ml), there was a decrease in IL-4-induced IL-5 expression without differences in both groups, indicating an intact T(H)2 response to bacterial endotoxin LPS in asthma. Interestingly, LPS increased the IL-12-induced INF-gamma release in a concentration-dependent manner in T-lymphocytes of normals but this could not be found in T cells of asthmatics, indicating an impaired T(H)1 response to bacterial endotoxin LPS in asthma. In addition, there was a TLR 4 expression on CD4(+) T-lymphocytes of normals and to a lesser extent in asthmatics but this TLR 4 expression could not be found on CD8(+) T cells of both groups. In conclusion, there may be an impaired concentration-dependent LPS-induced T(H)1 rather than a T(H)2 response in allergic adult asthmatics compared with normal volunteers. One reason for this could be a reduced TLR 4 expression on CD4(+) T-lymphocytes of asthmatic subjects.
机译：流行病学证据，体外研究和动物模型表明，暴露于细菌内毒素脂多糖（LPS）会影响哮喘的发展和严重程度。尽管已知通过Toll样受体（TLR）进行信号传递是适应性T辅助细胞1和2应答所必需的，但尚不清楚LPS配体TLR 4是否在CD4（+）和CD8（+）T-上表达在这种情况下，LPS是否可以调节T（H）1或T（H）2反应。因此，本作者使用RT-PCR方法和FACS分析检查了TLR 4在外周血CD4（+）和CD8（+）T淋巴细胞上的表达。此外，作者研究了在存在的情况下IL-12诱导的T（H）1相关细胞因子INF-γ的表达和IL-4-诱导的T（H）2特异性细胞因子IL-5的表达。使用ELISA检测LPS并比较9名特应性哮喘受试者和11名非特应性正常志愿者。与正常人相比，哮喘患者T细胞中抗CD3 /抗CD28诱导的IL-5表达增加（p <0.01）。在存在IL-4（10 ng / ml）的情况下，与哮喘患者相比，正常人T细胞中IL-5的表达进一步增加（p <0.05）。在抗CD3 /抗CD28诱导的T淋巴细胞中有INF-γ的表达，两组之间无差异（NS）。在存在IL-12（10 ng / ml）的情况下，INF-γ释放增加，而正常人与哮喘病（NS）之间没有差异。在存在不同浓度的LPS（10 ng / ml，1杯/ ml）的情况下，IL-4诱导的IL-5表达下降，两组均无差异，表明对T（H）2的完整反应哮喘中细菌内毒素LPS。有趣的是，LPS以正常浓度的方式增加了正常人T淋巴细胞中IL-12诱导的INF-γ释放，但在哮喘患者的T细胞中未发现这点，表明对细菌内毒素的T（H）1反应受损哮喘中的LPS。另外，正常人的CD4（+）T淋巴细胞上有TLR 4表达，哮喘患者中有较少的TLR 4表达，但两组的CD8（+）T细胞上均没有这种TLR 4表达。总之，与正常志愿者相比，在过敏性成人哮喘患者中可能存在浓度依赖的LPS诱导的T（H）1而非T（H）2应答受损。原因之一可能是哮喘受试者的CD4（+）T淋巴细胞上的TLR 4表达降低。

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