哮喘小鼠肺组织中CXC趋化因子受体3和其配体干扰素-γ诱导蛋白-10的表达及意义

Expressions of Chemokine Receptor CXCR3 and Its Ligand Interferon-γ-Inducible Protein-10 in Lung Tissue of Asthmatic Model Mice and Their Significances

目的观察CXC趋化因子受体3(CXCR3)及配体IFN-γ诱导蛋白-10(IP-10)在哮喘小鼠肺组织中的表达,探讨地塞米松(DEX)、卡介苗(BCG)干预对其表达的影响。方法健康雄性昆明小鼠40只,分为哮喘组、DEX组、BCG组和对照组,每组10只。哮喘组分别于实验第1、3、5、7、9、11、13天腹腔注射卵清蛋白(OVA)10μg致敏,第21天起予10g/LOVA5mL雾化吸入30min,1次/d,连续7d,激发哮喘。DEX组在雾化吸入前30min,按2mg/kg腹腔注射DEX溶液。BCG组在致敏前7、3、1d分别皮内注射BCG0.025mg。对照组用9g/L盐水代替OVA。各组小鼠于末次雾化吸入24h后麻醉并处死,取其肺组织置于40g/L多聚甲醛中固定,48h后取出,石蜡包埋、切片、HE染色。免疫组织化学法检测各组小鼠肺组织中CXCR3、IP-10蛋白的表达。结果4组间小鼠肺组织中CXCR3蛋白表达有显著性差异(F=4.602P=0.008),IP-10表达亦有显著性差异(F=4.207P=0.012)。哮喘组小鼠肺组织CXCR3、IP-10蛋白表达较对照组明显增加(Pa=0.002);DEX组CXCR3、IP-10蛋白表达较哮喘组明显降低(P=0.029,0.019);BCG组CXCR3、IP-10蛋白表达较哮喘组降低,但均无统计学意义。结论趋化因子受体CXCR3及配体IP-10参与哮喘发病过程,DEX与BCG可不同程度干预CXCR3、IP-10的表达。

Objective To observe the expressions of the chemokine receptor CXCR3 and its ligand IFN -γ- inducible protein - 10 （IP - 10） in lung tissue of asthmatic model mice and to explore further the effect of dexamethasone（DEX） and bacillus Calmette - Guerin vaccine （BCG） on the expressions of CXCR3 and IP - 10. Methods Forty Kunming mice were randomly divided into 4 groups ： asthmatic group, DEX group,BCG group and control group, 10 in each group. Mice were sensitized and challenged with ovalbumin （OVA） to establish asthmatic models. Ten mice in DEX group were administrated DEX （2 mg/kg） by abdomen injection 30 min before challenge （DEX group）. Ten mice in BCG group were injected BCG（0.025 mg） intradermally 7,3, and 1 days before sensitization. The mice in control group mice were treated with 9 g/L saline instead of OVA. Mice of each group were executed 24 hours after the final challenge. Their lung tissue were paraffin embedded, sliced and stained by HE. The expressions of CXCR3 and IP - 10 protein in lung tissue of mice were detected by immunohistochemistry. Results Distinct differences were discovered in the expressions of CXCR3 （ F- 4. 602 P = 0. 008 ） and IP - 10 （ F = 4. 207 P = 0. 012） among the 4 groups. The expressions of CXCR3 and IP - 10 in lung tissue of mice in asthmatic group were significantly higher than those in Control group （Pn = 0. 002） ,while that in DEX group were significantly lower than that in asthmatic group （P = 0. 029,0. 019 ）. There were no significant difference between the BCG group and asthmatic group. Conclusions The chemokine receptor CXCR3 and its ligand IP - 10 play an important roles in mechanisms in the pathogenesis of asthma. DEX and BCG can interfere the expressions of CXCR3 and IP - 10 in varying degress.