Toll样受体2介导的JNK信号分子在小鼠支气管哮喘发病中的作用机制  

Mechanism of c-Jun N-terminal kinase mediated by Toll like receptor 2 in murine asthma

作　　者：沈佩婷 方磊[1] 吴惠梅[1] 沈启英[1] 何芳[1] 刘荣玉[1] 

机构地区：[1]安徽医科大学第一附属医院干部呼吸科,安徽省老年病研究所,合肥230022

出　　处：《安徽医科大学学报》2015年第5期573-576,共4页Acta Universitatis Medicinalis Anhui

基　　金：国家自然科学基金(编号:81270082;81170030;81300027);高等学校博士学科点专项科研基金(编号:20113420110006);安徽省重点实验室计划项目(编号:1206c0805028);安徽省科技攻关项目(编号:12010402135)

摘　　要：目的探讨Toll样受体2(TLR2)介导的c-Jun氨基末端激酶(JNK)信号分子参与小鼠支气管哮喘发病的作用机制。方法健康SPF级C57(TLR2野生型)鼠和TLR2基因缺失(TLR2-/-)鼠各14只,按随机数字表法分为4组:C57对照组、C57哮喘组、TLR2-/-对照组、TLR2-/-哮喘组,每组7只,哮喘组以卵清蛋白(OVA)腹腔注射联合雾化吸入致敏和激发建立哮喘模型,对照组以生理盐水代替OVA致敏和激发。利用免疫组织化学染色技术(ABC法)检测TLR2蛋白在C57对照组、C57哮喘组肺内的表达差异,JNK及磷酸化JNK(P-JNK)蛋白表达在各组肺内的表达差异。结果 HE染色提示较其余3组,C57哮喘组有较明显的炎症细胞浸润及呼吸道平滑肌增生。以平均吸光度(m A)衡量各组织蛋白相对表达量,免疫组化结果提示TLR2蛋白在C57哮喘组表达显著高于C57对照组(P<0.01),JNK蛋白在各组的表达差异无统计学意义,P-JNK蛋白在C57哮喘组肺组织的表达量显著高于C57对照组、TLR2-/-哮喘组、TLR2-/-对照组(F=43.261,P<0.01)。结论 TLR2介导的JNK信号分子通路可能参与了支气管哮喘的发病过程。Objective To explore the mechanism of c-Jun N-terminal kinase mediated by Toll like receptor 2 in murine asthma. Methods 14 healthy SPF grade C57 wild-type mice and 14 TLR2 knockout （TLR2 ^- / - ） mice were randomly divided into four groups： C57 control group, C57 asthma group, TLR2 ^- / - control group, TLR2^ - / - asth-ma group （n = 7）. We utilized intraperitoneal injection combined with inhalation of ovalbumin （OVA） to sensitize and challenge the mice, thus establishing the experimental models of asthma. Meanwhile, the control group received normal saline instead of OVA. The protein expression of TLR2 was detected by immunohistochemistry（ABC meth-od） in C57 control group and C57 asthma group,as well as JNK and phosphorylation c-Jun（P-JNK） between each group. Results In C57 asthma group,HE-staining showed more obvious inflammatory cell infiltration around bron-chi and airway smooth muscle hyperplasia than the other three groups. The relative protein expressions were meas-ured by mean absorbance（mA）. Immunohistochemistry indicated that mean absorbance values of TLR2 was signifi-cantly higher in C57 asthma group than those of C57 control group （P 〈 0. 01）. There was no obvious difference of JNK protein expression between each group. The immunoexpression of P-JNK in C57 asthma group was notablely higher than those of C57 control group, TLR2 ^- / - asthma group, TLR2 ^- / - control group （F = 43. 261,P 〈 0. 01）. Conclusion TLR2-mediated JNK signaling molecules may be involved in the process of murine asthma.

关 键 词：哮喘 TLR2 JNK P—JNK 免疫组化 

分 类 号：R562.25[医药卫生—呼吸系统] Q241[医药卫生—内科学]