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首页> 外文期刊>Allergy >Omalizumab decreases nonspecific airway hyperresponsiveness in vitro.
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Omalizumab decreases nonspecific airway hyperresponsiveness in vitro.

机译：奥马珠单抗可降低体外非特异性气道高反应性。

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Background: In asthmatic patients, both symptoms and hyperresponsiveness are related to immunoglobulin E (IgE) concentration in serum. The anti-IgE monoclonal antibody omalizumab improved the control of asthma, but its effect on airway hyperresponsiveness is controversial. Passive sensitization reproduced in vitro a bronchial hyperresponsiveness, an increase in IgE bearing cells, and a mast cell degranulation. This study was designed to examine the effect of omalizumab on passive sensitization-induced hyperresponsiveness, alterations in IgE positive inflammatory cells and mast cell degranulation within the bronchial wall. Methods: Proximal (3-5 mm diameter) and distal (0.5-1.5 mm diameter) human bronchi dissected out from 10 lung specimens were incubated in normal or asthmatic serum containing various concentrations of omalizumab. Contractile responses to histamine or Dermatophagoides pteronyssinus (D. pter) were recorded using an organ bath system and expressed as percentage of maximal contractile response to acetylcholine (ACh). Immunohistochemistry was performed using monoclonal antibodies directed against IgE or tryptase. Mast cells were classified as fully granulated (type I), partly (type II) or largely degranulated (type III). Results: The specific bronchial hyperresponsiveness to D. pter and the nonspecific bronchial hyperresponsiveness to histamine following passive sensitization were significantly inhibited by omalizumab in both distal and proximal airways. Passive sensitization-induced increase in IgE positive cells was also abolished by omalizumab in a concentration dependent manner. Mast cell degranulation which was inhibited by omalizumab was positively correlated with the contractile response to D. pter. Conclusions: Omalizumab blocks specific and nonspecific bronchial hyperresponsiveness. Anti-IgE also decreases IgE bearing cell number and mast cell degranulation.
机译：背景：在哮喘患者中，症状和反应过度都与血清中免疫球蛋白E（IgE）浓度有关。抗IgE单克隆抗体omalizumab改善了哮喘的控制，但其对气道高反应性的作用尚存争议。被动致敏在体外重现了支气管高反应性，携带IgE的细胞增加以及肥大细胞脱粒。这项研究旨在检查omalizumab对被动致敏引起的反应过度，IgE阳性炎症细胞改变和支气管壁肥大细胞脱粒的影响。方法：将从10个肺标本中切出的近端（直径3-5毫米）和远端（直径0.5-1.5毫米）人支气管在含有各种浓度的omalizumab的正常或哮喘血清中孵育。使用器官浴系统记录对组胺或鹿角皮癣（D.pter）的收缩反应，并表示为对乙酰胆碱（ACh）的最大收缩反应的百分比。免疫组织化学使用针对IgE或类胰蛋白酶的单克隆抗体进行。肥大细胞分为完全颗粒化（I型），部分颗粒化（II型）或大部分颗粒化（III型）。结果：omalizumab在远端和近端气道中显着抑制了被动致敏后对D. pter的特异性支气管高反应性和对组胺的非特异性支气管高反应性。奥马珠单抗也以浓度依赖性的方式消除了被动致敏引起的IgE阳性细胞增加。 omalizumab抑制的肥大细胞脱粒与对D. pter的收缩反应呈正相关。结论：奥马珠单抗可阻断特异性和非特异性支气管高反应性。抗IgE还可减少IgE轴承细胞数和肥大细胞脱粒。

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