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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >IgE/antigen-mediated enhancement of IgE production is a mechanism underlying the exacerbation of airway inflammation and remodelling in mice
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IgE/antigen-mediated enhancement of IgE production is a mechanism underlying the exacerbation of airway inflammation and remodelling in mice

机译：IgE /抗原介导的IgE产生增强是小鼠气道炎症加剧和重塑的基础机制

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摘要

IgE is known to enhance some antibody responses to specific antigens, but whether this contributes to allergic asthma remains unclear. We have previously found that repeated antigen challenges in mice sensitized with antigen-specific IgE monoclonal antibody (mAb) exacerbated airway inflammation and remodelling accompanied by increased levels of endogenous antigen-specific IgE and IgG1. Here, we investigated whether IgE/antigen-mediated enhancement of endogenous IgE production contributes to the exacerbation of airway inflammation and remodelling. BALB/c mice passively sensitized with ovalbumin (OVA) -specific IgE mAb were challenged with OVA intratracheally seven times; anti-IgE mAb was intraperitoneally administered 1day before the fourth challenge. Treatment with anti-IgE mAb inhibited the increased level of endogenous OVA-specific IgE in serum, but not OVA-specific IgG1, and a biphasic increase in airway resistance at the fourth challenge. Furthermore, a biphasic increase in airway resistance, airway hyper-responsiveness to methacholine, OVA-specific IgE and IgG1 production, and infiltrations by neutrophils and eosinophils in the lungs at the seventh challenge were suppressed by treatment; airway remodelling, such as goblet cell hyperplasia and sub-epithelial fibrosis, was also reduced. In addition, the production of interleukin-17A, interleukin-33 and CXCL1 in the lungs related to these IgE-mediated responses was decreased by treatment. Collectively, we found that the mechanism leading to the exacerbation of allergic asthma is closely related to IgE/antigen-mediated enhancement of IgE production, suggesting that this may create a vicious circle leading to the chronic status in asthmatic patients having levels of antigen-specific IgE ready to form complexes with antigen.
机译：众所周知，IgE可以增强对特定抗原的某些抗体反应，但是尚不清楚这是否会导致过敏性哮喘。我们以前已经发现，用抗原特异性IgE单克隆抗体（mAb）致敏的小鼠反复进行抗原挑战会加剧气道炎症和重塑，并伴有内源性抗原特异性IgE和IgG1水平升高。在这里，我们调查了IgE /抗原介导的内源性IgE产生的增强是否有助于气道炎症的加剧和重塑。被动给予卵清蛋白（OVA）特异性IgE mAb致敏的BALB / c小鼠气管内用OVA攻击7次;在第四次攻击前1天腹膜内施用抗IgE mAb。用抗IgE单抗治疗可抑制血清中内源性OVA特异性IgE的水平升高，但不能抑制OVA特异性IgG1的水平，并且在第四个挑战时气道阻力呈双相增加。此外，在第七次挑战中，通过治疗抑制了气道阻力的双相增加，气道对乙酰甲胆碱的过度反应，OVA特异性IgE和IgG1的产生以及中性粒细胞和嗜酸性粒细胞在肺部的浸润。气道重塑，如杯状细胞增生和上皮下纤维化也减少了。另外，通过治疗减少了与这些IgE介导的反应相关的肺中白介素17A，白介素33和CXCL1的产生。总的来说，我们发现导致过敏性哮喘恶化的机制与IgE /抗原介导的IgE产生增加密切相关，这表明这可能会导致恶性循环，导致具有抗原特异性水平的哮喘患者的慢性状态IgE准备与抗原形成复合物。

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