过敏性哮喘患者的气道IL-6水平独立于炎症,但与气道功能下降相关

2010/07/05

    背景:哮喘为气道慢性炎症性疾病,主要表现为Th2型免疫反应。越来越多的证据表明Th17细胞参与了哮喘的发病过程。IL-6能使效应T细胞亚群增加,这表明IL-6参与了哮喘的发生过程。通常将IL-6与THFα和IL-1β一起归为炎症标记物,而非调节性细胞因子。
    目的:研究过敏性哮喘中IL-6与其他促炎细胞因子、Th2/Th17细胞因子和肺功能之间的关系,评价IL-6在过敏性哮喘中的作用。
    方法:对16名健康对照和18名轻至中度过敏性哮喘患者检测诱导痰液中细胞因子水平和肺功能。
    结果:促炎因子(THFα和IL-1β)水平在对照组和哮喘患者组未见显著性差异。相反,与健康对照相比,IL-6水平在哮喘患者显著增加(P<0.01)。整个队列研究的等级回归分析显示,IL-6介导了哮喘和肺功能的相关性。Th2细胞因子中,仅IL-13(P<0.05)在哮喘患者显著增加,而且与IL-6水平成正相关(rS=0.53, P<0.05)。
    结论:对于轻至中度哮喘患者,IL-6独立于其他促炎生物标记物,同时IL-6与IL-13存在相关。此外,IL-6可能导致过敏性哮喘患者肺功能受损。
(刘国梁 审校)
Neveu WA, et al. Respir Res. 2010 Mar 8;11(1):28. [Epub ahead of print]
 

Elevation of IL-6 in the allergic asthmatic airway is independent of inflammation but associates with loss of central airway function.

 

Neveu WA, Allard JL, Raymond DM, Bourassa LM, Burns SM, Bunn JY, Irvin CG, Kaminsky DA, Rincon M.
 
BACKGROUND: Asthma is a chronic inflammatory disease of the airway that is characterized by a Th2-type of immune response with increasing evidence for involvement of Th17 cells. The role of IL-6 in promoting effector T cell subsets suggest that IL-6 may play a functional role in asthma. Classically IL-6 has been viewed as an inflammatory marker, along with TNFalpha and IL-1beta, rather than as regulatory cytokine.
OBJECTIVE: To investigate the potential relationship between IL-6 and other proinflammatory cytokines, Th2/Th17 cytokines and lung function in allergic asthma, and thus evaluate the potential role of IL-6 in this disease.
METHODS: Cytokine levels in induced sputum and lung function were measured in 16 healthy control and 18 mild-moderate allergic asthmatic subjects.
RESULTS: The levels of the proinflammatory biomarkers TNFalpha and IL-1beta were not different between the control and asthmatic group. In contrast, IL-6 levels were specifically elevated in asthmatic subjects compared with healthy controls (p<0.01). Hierarchical regression analysis in the total study cohort indicates that the relationship between asthma and lung function could be mediated by IL-6. Among Th2 cytokines only IL-13 (p<0.05) was also elevated in the asthmatic group, and positively correlated with IL-6 levels (rS=0.53, p<0.05).
CONCLUSIONS: In mild-moderate asthma, IL-6 dissociates from other proinflammatory biomarkers, but correlates with IL-13 levels. Furthermore, IL-6 may contribute to impaired lung function in allergic asthma.
 
 


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