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Allergen provocation increases TH2-cytokines and FOXP3 expression in the asthmatic lung

机译：过敏原激发增加哮喘肺中TH2-细胞因子和FOXP3表达

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Background: Allergic asthma is caused by allergen-specific IgE and T-helper cell (Th) type 2 responses towards airborne allergens. The objective of this study was to investigate local and systemic regulatory mechanisms in the early asthmatic response to bronchial allergen provocation.Methods: Birch pollen-allergic patients with mild asthma (n = 13) and healthy non-allergic controls (n = 14) were subjected to bronchoalveolar lavage (BAL) and blood sampling. On patients BAL was performed twice: without preceding provocation ('before samples') and 24 h after bronchial provocation with birch pollen allergen. Lymphocytes in BAL and peripheral blood mononuclear cells (PBMCs) were phenotyped by multi-colour flow cytometry and cytokines measured by cytometric bead array. Proliferation and secreted cytokines were analysed in allergen-stimulated PBMCs, CD25~+ depleted PBMCs and PBMCs with IL-10 neutralizing antibodies. Results: The numbers of CD69~+ and FOXP3~+ lymphocytes were higher in BAL after compared with before allergen provocation in asthmatic patients. Moreover, allergen provocation increased expression of FOXP3 in CD4~+ CD25bnght cells. The cytokine profile in BAL fluid from asthmatics revealed higher levels of IL-5, compared with the controls, and an increase in IL-5, IL-6, IL-9 and IL-10 after allergen provocation. Pollen allergen stimulated PBMC cultures from asthmatic patients produced elevated levels of IL-5 and IL-13 compared with the controls, which were not affected by depletion of CD25~+ cells or IL-10 neutralization. Conclusion: Despite an increase in CD4~+ CD25brlght cells expressing high levels of FOXP3 in response to bronchial allergen provocation, asthmatic patients exhibit enhanced levels of Th2 cytokines in the lung, which may indicate an inability among infiltrating cells to suppress Th2 responses.
机译：背景：过敏性哮喘是由对空气传播的过敏原的过敏原特异性IgE和2型T辅助细胞（Th）反应引起的。这项研究的目的是探讨哮喘对支气管过敏原激发的早期和局部调节机制。方法：桦树花粉过敏的轻度哮喘患者（n = 13）和健康的非过敏对照（n = 14）进行支气管肺泡灌洗（BAL）和血液采样。对患者进行BAL两次：无前期刺激（“样本前”）和支气管激发后24h桦树花粉过敏原。通过多色流式细胞术对BAL和外周血单核细胞（PBMC）中的淋巴细胞进行表型分析，并通过流式细胞仪检测细胞因子。分析了过敏原刺激的PBMC，CD25〜+耗尽的PBMC和带有IL-10中和抗体的PBMC的增殖和分泌的细胞因子。结果：哮喘患者BAL后CD69〜+和FOXP3〜+淋巴细胞数量高于过敏原激发前。此外，过敏原激发增加了FOXP3在CD4〜+ CD25bnght细胞中的表达。与对照组相比，哮喘患者的BAL液中的细胞因子谱显示较高的IL-5水平，并且在过敏原激发后IL-5，IL-6，IL-9和IL-10升高。与对照组相比，哮喘患者的花粉变应原刺激的PBMC培养物产生的IL-5和IL-13水平升高，不受CD25〜+细胞耗竭或IL-10中和的影响。结论：尽管响应支气管变应原激发，表达高水平FOXP3的CD4〜+ CD25brlght细胞增加，哮喘患者的肺Th2细胞因子水平升高，这可能表明浸润细胞无法抑制Th2反应。

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