先天免疫激活在中性粒细胞性哮喘及支气管扩张中的作用
2007/06/27
先天免疫在哮喘发病机制中的作用尚未阐明，但可能与哮喘的特异质炎症反应有关。细菌脂多糖、病毒感染和颗粒物可刺激先天免疫受体而激活炎症反应，包括白介素-8（IL-8）的释放和中性粒细胞的浸润.。目前已证实存在非嗜酸性粒细胞性哮喘（即有哮喘症状发作和气道高反应性而痰液中嗜酸性粒细胞不增高），如中性粒细胞性哮喘，但其发病机制还不甚清楚。Jodie L Simpson等通过对49名不抽烟成人哮喘患者（美国胸科协会诊断标准）、9名支气管扩张患者（高分辨CT证实）及13名健康者（FEV1＞80％预计值）诱导痰中先天免疫受体（包括Toll样受体(TLR)2、TLR4、CD14及炎症因子等）和表面活性蛋白A、IL-8、可溶性CD14及内毒素水平的检测，力图阐明先天免疫应答激活是否参与以IL-8升高为特征的中性粒细胞性哮喘的炎症反应机制。结果发现：支气管扩张组和中性粒细胞性哮喘组受试者的先天免疫受体TLR2、TLR4、CD14和炎症因子IL-8、IL-1β表达较其他哮喘亚组（即非中性粒细胞性哮喘组）及对照组显著增加。中性粒细胞性哮喘组受试者气道内毒素水平较其他各组增高。所以作者初步认为：先天免疫系统激活可导致哮喘促炎细胞因子的产生和释放，并可能参与中性粒细胞性哮喘的发病机制。
（戴元荣 温州医学院附属第二医院呼吸内科 325027 摘译）
(Thorax. 2007. 62:211–218)
Author：Jodie L Simpson, Terry V Grissell, Jeroen Douwes, Rodney J Scott, Michael J Boyle, Peter G Gibson
Institution：Department of Respiratory and Sleep Medicine, School of Medicine and Public Health,Hunter Medical Research Institute, The University of Newcastle, Newcastle,Australia
Title：Innate immune activation in neutrophilic asthma and bronchiectasis
Source：Thorax 62:211–218, March 2007.
Abstract
Background: The role of the innate immune system in the pathogenesis of asthma is unclear. Activation of innate immune receptors in response to bacterial lipopolysaccharide, viral infection and particulate matter triggers a pre-programmed inflammatory response, which involves interleukin (IL)8 and neutrophil influx. The inflammatory response in asthma is heterogeneous.Aim: To test the hypothesis that innate immune activation may be a relevant inflammatory mechanism in neutrophilic asthma where IL8 levels are increased.
Methods: Induced sputum was obtained from non-smoking adults with asthma (n=49), healthy controls (n=13) and a positive reference group with bronchiectasis (n=9). Subjects with asthma were classified into inflammatory subtypes using induced sputum cell counts. Sputum was examined for mRNA expression of the innate immune receptors toll-like receptor (TLR)2, TLR4 and CD14, and inflammatory cytokines. A separate sputum portion was dispersed and the supernatant assayed for surfactant protein A, IL8, soluble CD14 and endotoxin.
Results: Expression of innate immune receptors was increased in subjects with bronchiectasis and neutrophilic asthma compared with other asthma subtypes and controls. Increased expression of the receptors TLR2, TLR4 and CD14, as well as the pro-inflammatory cytokines IL8 and IL1b, was observed. Subjects with neutrophilic asthma had higher airway levels of endotoxin than the other groups studied.
Conclusion: There is evidence of activation of the innate immune system in asthma which results in the production of pro-inflammatory cytokines and may contribute to the pathogenesis of neutrophilic asthma.
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重新认识β2受体基因多态性与哮喘的关系
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吸烟引起哮喘支气管粘膜免疫状态改变
