白细胞介素33在支气管哮喘急性加重中的作用  

Roles of interleukin-33 in bronchial asthma acute exacerbation

作　　者：何杨 赵云霞[1] He Yang;Zhao Yunxia(The First Department of Respiratory Medicine,the Third Hospital of Hebei Medical University,Shijiazhuang 050051,China)

机构地区：[1]河北医科大学第三医院呼吸一科,石家庄050051

出　　处：《国际呼吸杂志》2022年第12期944-948,共5页International Journal of Respiration

摘　　要：支气管哮喘是常见的慢性呼吸道疾病,大多数情况下哮喘急性发作与接触过敏原、病毒性上呼吸道感染、空气污染、吸烟相关。白细胞介素33(IL-33)是IL-1的家族成员,从基因、动物实验模型、临床上均已证明IL-33与哮喘密切相关。肺组织中的结构细胞以及被趋化因子招募至肺组织的游离细胞通过一系列模式识别受体、传导介质、传导轴,诱导IL-33的产生、释放,进一步导致辅助型T细胞1型免疫反应减弱、辅助型T细胞2型免疫反应增强,哮喘症状加重。阐明IL-33的释放机制可以为认识哮喘急性发作及精准靶向治疗支气管哮喘提供新的思路。本文对支气管哮喘急性加重过程中IL-33的产生、释放机制作一综述。Bronchial asthma is a common chronic respiratory disease.In most cases,the acute attack of asthma is related to exposure to allergens,upper respiratory viral infection,air pollution,and smoking.Interleukin-33,a member of the interleukin-1 family,has been proved to be closely related to asthma from the perspectives of gene,animal experimental model,and clinical practice.Structural cells in lung tissue and free cells recruited by chemokines to lung tissue induce interleukin-33 production and release through a series of pattern recognition receptors,conduction mediators,and conduction axes.The results further lead to a weakened T helper 1 cell type immune response and an enhanced T helper 2 cell type immune response,exacerbating asthma symptoms.Elucidating the release mechanism of interleukin-33 can provide new ideas for understanding the acute attack of asthma and for precisely targeted treatment of bronchial asthma.This article reviews the mechanism of interleukin-33 production and release during acute exacerbation of bronchial asthma.

关 键 词：哮喘 白细胞介素33 释放机制 

分 类 号：R562.25[医药卫生—呼吸系统]