寒冷刺激致小鼠上呼吸道黏膜免疫功能低下模型的研究

A mouse model of upper respiratory tract mucosal immunity dysfunction induced by cold stimulation

目的:探索建立寒冷刺激致小鼠上呼吸道黏膜免疫功能低下模型。方法:将昆明种小鼠置于-20℃寒冷环境中,分别给予5 min、10 min、15 min、20 min 4个时段的寒冷刺激,以小鼠唾液分泌型免疫球蛋白A(SIgA)含量和溶菌酶活性作为关键检测指标,评价模型的建立是否成功。结果:20 min组小鼠出现50%的动物死亡;15 min组小鼠SIgA含量及溶菌酶活性明显降低(P<0.05,P<0.01);10 min组小鼠仅出现溶菌酶活性降低(P<0.05);5 min组小鼠则各项指标均无显著差异(P>0.05)。结论:将小鼠置于-20℃寒冷环境中15 min,能成功建立上呼吸道黏膜免疫功能低下模型。

AIM： To establish a mouse model of upper respiratory tract mucosal immunity dysfunction induced by cold stimulation. METHODS： Mice were stimulated with cold by placing the animals in -20℃environment for 5 min, 10 min, 15 min or 20 min. The secretory immunoglobulin A（SIgA） level and lysozyme activity in the mouse saliva were determined for qualification. RESULTS： The mortality rate was 50% in the group of cold stimulation for 20 rain. Compared with the control mice, the SIgA level and lysozyme activity significantly decreased in the group of cold stimulation for 15 min （P 〈 0. 05 and P 〈 0.01, respectively）. Decreased lysozyme activity was only observed in the group of cold stimulation for 10 min （P 〈0105）. The data in the group of cold stimulation for 5 min were almost similar to those in control group. CONCLUSION： A mouse model of upper respiratory tract mucosal immunity dysfunction was successfully established by cold stimulation.