Toll样受体1和3在大鼠哮喘中的表达及甲泼尼龙对其的调控作用

目的观察Toll样受体(TLR)1和TLR3在哮喘大鼠中的表达及甲泼尼龙对其的影响,探讨TLRs在哮喘炎症过程中的可能作用机制。方法采用大鼠哮喘模型,随机分成哮喘组、对照组和甲泼尼龙组,流式细胞术检测血中性粒细胞TLR1的表达,免疫组织化学法检测肺组织TLR3的表达。结果哮喘组肺组织TLR3的吸光度值(A值)(0.20±0.03)与对照组(0.14±0.04)差异有统计学意义(P<0.01);甲泼尼龙组A值(0.20±0.04)分别与哮喘组和对照组差异无统计学意义(均P>0.05)。哮喘组中性粒细胞TLR1的平均荧光强度(MFI)(74.1±6.3)与对照组中性粒细胞TLR1的平均荧光强度(84.4±5.0)差异有统计学意义(P<0.01);甲泼尼龙组MFI(77.8±1.1)与哮喘组差异无统计学意义(P>0.05),但与对照组差异有统计学意义(P<0.05)。肺组织TLR3和血中性粒细胞TLR1蛋白表达水平呈负相关(r=-0.493,P<0.05)。结论哮喘大鼠肺组织TLR3蛋白的表达升高,血中性粒细胞TLR1蛋白的表达水平则反之,两者呈负相关。甲泼尼龙对它们具有调控趋势,但强度不是很明显。TLRs的表达过度或不足可能是哮喘急性发作的重要原因之一。

Expression of Toll-like receptor 1 and 3 in rat asthma models and regulation by methylprednisolone

Objective To investigate the expression of Toll-like receptor 1 and 3 （TLR1/TLR3） and the effects of methylprednisolone, and to explore the potential mechanisms responsible for the inflammatory responses triggered in rat asthma models. Methods The rat asthma models were, following successful construction, randomly assigned to asthma group, control group and methylprednisolone treatment group. This entailed measurement of the level of TLR1 in blood neutrophils by using flow cytometry and expression of TLR3 by using immunohistochemical assay. Results The level of TLR1 at blood neutrophil in asthma model group was significantly lower than that in control group （74.1± 6.3） MFI vs （84.4±5.0） MFI, P〈0.01）. The difference in TLR1 at blood neutrophil between asthma model group and methylprednisolone treatment group （77.8±1.1） MFI, P〉O.05]. Despite that the optical density of TLR3 in lung tissues in asthma model group was significantly higher than that in control group （0.20±0.03） vs （0.14±0.04）, P〈0.01], their difference with methylprednisolone treatment group （0.20±0.04） was unremarkable （both P〉0.05）. There was a remark- able negative correlation between TLR1 at blood neutrophil and TLR3 in lung tissue （r=-0.493, P〈0.05）. Conclusion In mice asthma model, the expression of TLR3 is up-regulated the lung tissue yet TLR1 is down-regulated in blood neutrophils, with an observed negative correlation. Methylprednisolone has a modest but insignificant regulatory effect on TLR1/3 expression. TLRs over-expression or under-expression may be an important pathogenesis of asthma exacer- bation.