TLR4信号转导途径在年幼期哮喘大鼠气道炎症中的作用  

Effect of Toll-like receptor 4 signal transduction on airway inflammation in infant asthmatic rat

作　　者：苏苗赏[1] 徐漫欢[2] 李昌崇[1] 陈福将[1] 管小俊[1] 郑仰明[1] 张海邻[1] 罗运春[1] 

机构地区：[1]温州医学院附属育英儿童医院呼吸科,浙江温州325027 [2]温州医学院附属第二医院神经内科,浙江温州325027

出　　处：《中国病理生理杂志》2008年第1期15-19,共5页Chinese Journal of Pathophysiology

基　　金：浙江省自然科学基金资助项目(No.Y205426)

摘　　要：目的:研究哮喘大鼠Toll样受体4(TLR4)表达变化及其对嗜酸性粒细胞(EOS)凋亡的作用机制。方法:清洁级SD大鼠27只,随机分为对照组(A)、哮喘组(B)、地塞米松(D)组,每组9只。用OVA致敏与激发复制哮喘模型。光镜观察肺组织病理变化;BALF中炎症细胞计数;ELISA测定血清IL-10含量;原位杂交测定肺组织TLR4mRNA表达;TUNEL法检测EOS凋亡。结果:(1)光镜观察:B组见肺组织大量炎症细胞侵润,支气管黏液腺增生;D组上述现象明显减轻。(2)BALF中细胞总数、EOS绝对计数和EOS占细胞总数的百分比:B组均明显高于A组(均P<0.01);D组均明显低于B组(均P<0.01)。(3)血清IL-10含量:B组与A组有显著差异(P<0.01);D组显著低于B组(P<0.01)。(4)TLR4mRNA的检测:TLR4在肺组织表达B组与A组差异无统计学意义(P>0.05);D组显著高于B组(P<0.01)。(5)EOS凋亡率检测结果,B组与A组比差异显著(P<0.05);D组显著高于B组(P<0.01)。相关分析显示,TLR4mRNA表达与EOS凋亡率呈显著正相关(r=0.612,P<0.01)。结论:DXM上调血清中IL-10水平,诱导肺组织EOS凋亡,可能与TLR4信号通路有关。AIM ： To study the change and regulatory mechanism of Toll - like receptor 4 （TLR4） on eosinophil （EOS） apoptosis. METHODS： Twenty -seven SD rats were randomly divided into control group （A） , asthma group （B） and dexamethasone group （D）. Asthmatic model rats were sensitized and repeatedly exposed to aerosolized ovalbumin. Pulmonary tissues were observed under light microscope （LM）. The inflammatory cells in BALF were counted. The levels of IL - 10 in serum were measured by ELISA. Expressions of TLR4 mRNA were tested by hybridization. The apoptotic EOS was detected by TUNEL. RESULTS： （ 1 ） LM showed that inflammatory cells infiltrated around the bronchus, airway mucous plug in group B, obviously lightened in group D. （2） Inflammatory cells count in BALF： the total cellular score, EOS absolute count and EOS% in group B were significantly increased （P 〈0. 01 ）. Compared to group B, a significant decrease in group D was observed （ P 〈 0.01 ）. （3） The level of IL - 10 in group B was significantly higher than that in group A and in group D （ P 〈 0. 01 ）. （4） No significant difference （ P 〉 0. 05 ） of TLR4 mRNA expression was observed between group A and group B. However, that in group D were significantly increased （ P 〈 0. 01 ）. （5） Percentages of apoptotic EOS in group B were significantly lower than those in group A （ P 〈 0. 01 ）, those in group D were significantly increased （P 〈 0. 01 ）. A significant correlation between TLR4 mRNA and apoptotic EOS （ r = 0. 612, P 〈 0. 01 ） was observed. CONCLUSION： Dexamethasone can increase IL- 10 secretion, induce EOS apoptosis, which may correlate with TLR4 signal transduction.

关 键 词：受体 Toll样 白细胞介素10 嗜酸细胞 哮喘 地塞米松 

分 类 号：R392.32[医药卫生—免疫学]