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Can anti-IgE therapy prevent airway remodeling in allergic asthma?

机译：抗IgE疗法可预防过敏性哮喘中的气道重塑吗？

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摘要

Airway remodeling is a central feature of asthma. It is exemplified by thickening of the lamina reticularis and structural changes to the epithelium, submucosa, smooth muscle, and vasculature of the airway wall. Airway remodeling may result from persistent airway inflammation. Immunoglobulin E (IgE) is an important mediator of allergic reactions and has a central role in airway inflammation and asthma-related symptoms. Anti-IgE therapies (such as omalizumab) have the potential to block an early step in the allergic cascade and therefore have the potential to reduce airway remodeling. The reduction in free IgE levels following anti-IgE therapy leads to reductions in high-affinity IgE receptor (FcepsilonRI) expression on mast cells, basophils, and dendritic cells. This combined effect results in attenuation of several markers of inflammation, including peripheral and bronchial tissue eosinophilia and levels of granulocyte macrophage colony-stimulating factor, interleukin (IL)-2, IL-4, IL-5, and IL-13. Considering the previously demonstrated anti-inflammatory effects of anti-IgE therapy, along with results from a small study showing continued benefit after discontinuation of long-term treatment, a larger study to assess its effect on markers of airway remodeling is underway.
机译：气道重塑是哮喘的主要特征。可以通过网状板的增厚以及上皮，粘膜下层，平滑肌和气道壁脉管系统的结构改变来举例说明。气道重塑可能源于持续的气道炎症。免疫球蛋白E（IgE）是过敏反应的重要介体，在气道炎症和哮喘相关症状中起重要作用。抗IgE治疗（例如奥马珠单抗）可能会阻止过敏性级联反应的早期阶段，因此可能会减少气道重塑。抗IgE治疗后游离IgE水平的降低导致肥大细胞，嗜碱性粒细胞和树突状细胞上高亲和力IgE受体（FcepsilonRI）表达的降低。这种综合作用导致炎症的几种标记减弱，包括外周和支气管组织嗜酸性粒细胞增多以及粒细胞巨噬细胞集落刺激因子，白介素（IL）-2，IL-4，IL-5和IL-13的水平。考虑到先前已证明的抗IgE治疗的抗炎作用，以及一项小型研究的结果表明长期停药后仍可继续获益，因此正在进行一项更大的评估其对气道重塑标志物作用的研究。

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