白介素-1β致豚鼠气道高反应性作用机制的研究  

The mechanism study of interleukin-1β induced airway hyperresponsiveness in guinea pigs

作　　者：陈雪芹[1] 曹霞[1] 杨炯[1] 曹作炎[1] 刘珍连[1] 

机构地区：[1]武汉大学人民医院呼吸内科,武汉430060

出　　处：《中国免疫学杂志》2004年第10期708-710,716,共4页Chinese Journal of Immunology

摘　　要：目的 :探讨白介素 1β(IL 1β)导致气道高反应性的作用机制。 方法 :建立IL 1β导致的气道高反应性的豚鼠模型 ,研究内源性气道神经元释放的神经激肽在IL 1β导致气道高反应性中的作用。 结果 :IL 1β组组胺的PC2 0 值明显小于对照组 (P <0 0 1) ,表明吸入IL 1β后可导致气道高反应性 ;辣椒素预处理组组胺的PC2 0 值与对照组相比无显著性差异 (P >0 0 5 ) ,表明辣椒素预处理可完全抑制IL 1β导致气道高反应性 ;NK1 受体拮抗剂组组胺的PC2 0 值与IL 1β组相比有显著性差异 (P <0 0 5 ) ,表明NK1 受体拮抗剂能完全抑制IL 1β导致气道高反应性。 结论 :内源性气道神经元释放的神经激肽SP在IL 1β导致气道高反应性起主要作用。Objective:To explore the mechanism of interleukin-1β(IL-1β) induced AHR.Methods:The authors work out an original model of AHR induced by IL-1β administered intratracheally to guinea pigs,and investigate the effects of neurokinin released from intrinsic airway neurons on the development of this airway hyperresponsiveness,PC 20 values were significantly lower in animals given IL-1β than that in controls( P <0 01),suggesting AHR induced by IL-1β.There is no difference in PC 20 values between animals with capsaicin pretreatment and controls( P >0 05),showing complete inhibition of IL-1β induced AHR by capsaicin pretreatment.PC 20 values were significantly higher in animals with NK 1 receptor antagonist pretreatment than that in animals exposed to IL-1β( P <0 01),indicating NK 1 receptor antagonist inhibits AHR induced by IL-1β.Conclusion:SP released from intrinsic airway neurons play a prodominant role in the development of IL-1β induced AHR.

关 键 词：IL-1β 气道高反应性 组胺 豚鼠 白介素-1Β NK1受体 对照组 辣椒素 显著性差异 释放 

分 类 号：R562.25[医药卫生—呼吸系统] R743[医药卫生—内科学]