哮喘联盟

    背景：抗IgE抗体奥马单抗可以抑制哮喘患者的变应反应，这并不与炎症条件的变化直接相关。我们推测抗IgE抗体通过抑制气道炎症来发挥其作用。为此进行了一个随机，双盲，安慰剂对照实验研究抗IgE抗体对25例哮喘患者支气管活检中过敏原诱发的炎症的作用。
    方法：变应原诱发后24小时行支气管镜粘膜活检作为基线，抗IgE抗体治疗或安慰剂治疗12周后再行支气管镜粘膜活检。基线日、治疗第8周和12周行支气管激发实验和痰诱导。对过敏原的早期和晚期反应、PC20、支气管粘膜活检组织和痰中炎性细胞进行评估。
    结果：与安慰剂相比(P<0.002)，抗IgE抗体治疗后早期和晚期哮喘反应降低到15.3％和4.7％以下。这与痰中和活检粘膜中(15-2细胞/0.1毫米2)(P<0.003)嗜酸性粒细胞计数(4-0.5％)减少是一致的。此外，各组活检组织免疫球蛋白E +细胞均显著减少，而抗免疫球蛋白E组高亲和力IgE受体和CD4 +细胞减少。支气管激发实验PC20没有显著差异.
    结论：抗IgE抗体可减少哮喘患者对吸入反应原的反应，与支气管粘膜嗜酸性粒细胞，含免疫球蛋白E细胞减少是一致的，支气管激发实验PC20无改变。这表明抗IgE抗体治疗哮喘的作用可能是通过抑制嗜酸性粒细胞炎症和IgE承载细胞数目达到的。

（陈欣 审校）
van Rensen EL, et al. Allergy. 2008 Dec 12. [Epub ahead of print]

Eosinophils in bronchial mucosa of asthmatics after allergen challenge: effect of anti-IgE treatment.

van Rensen EL, Evertse CE, van Schadewijk WA, van Wijngaarden S, Ayre G, Mauad T, Hiemstra PS, Sterk PJ, Rabe KF.
Department of Pulmonology, Leiden University Medical Center, Leiden, the Netherlands.

Background: Anti-IgE, omalizumab, inhibits the allergen response in patients with asthma. This has not been directly related to changes in inflammatory conditions. We hypothesized that anti-IgE exerts its effects by reducing airway inflammation. To that end, the effect of anti-IgE on allergen-induced inflammation in bronchial biopsies in 25 patients with asthma was investigated in a randomized, double-blind, placebo-controlled study.
Methods: Allergen challenge followed by a bronchoscopy at 24 h was performed at baseline and after 12 weeks of treatment with anti-IgE or placebo. Provocative concentration that causes a 20% fall in forced expiratory volume in 1 s (PC(20)) methacholine and induced sputum was performed at baseline, 8 and 12 weeks of treatment. Changes in the early and late responses to allergen, PC(20), inflammatory cells in biopsies and sputum were assessed.
Results: Both the early and late asthmatic responses were suppressed to 15.3% and 4.7% following anti-IgE treatment as compared with placebo (P < 0.002). This was paralleled by a decrease in eosinophil counts in sputum (4-0.5%) and postallergen biopsies (15-2 cells/0.1 mm(2)) (P < 0.03). Furthermore, biopsy IgE+ cells were significantly reduced between both the groups, whereas high-affinity IgE receptor and CD4+ cells were decreased within the anti-IgE group. There were no significant differences for PC(20) methacholine.
Conclusion: The response to inhaled allergen in asthma is diminished by anti-IgE, which in bronchial mucosa is paralleled by a reduction in eosinophils and a decline in IgE-bearing cells postallergen without changing PC(20) methacholine. This suggests that the benefits of anti-IgE in asthma may be explained by a decrease in eosinophilic inflammation and IgE-bearing cells.