Department of Medicine, University Kiel, Kiel, Germany and Krankenhaus Grosshansdorf, Center for Pulmonology and Thoracic Surgery, Wöhrendamm 80, Grosshansdorf, Germany.
Allergy. 2011 Sep;66(9):1142-51. doi: 10.1111/j.1398-9995.2011.02617.x. Epub 2011 Jun 7.
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 (FcεRI) 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.
气道重塑是哮喘的一个主要特征。它的表现为网状层增厚和气道壁的上皮、黏膜下组织、平滑肌和血管的结构改变。气道重塑可能是由持续的气道炎症引起的。免疫球蛋白 E（IgE）是过敏反应的重要介质，在气道炎症和与哮喘相关的症状中起着核心作用。抗 IgE 疗法（如奥马珠单抗）有可能阻断过敏级联反应的早期步骤，因此有可能减少气道重塑。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（FcεRI）的表达减少。这种综合作用导致炎症的几个标志物减弱，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、白细胞介素 (IL)-2、IL-4、IL-5 和 IL-13 的水平降低。考虑到抗 IgE 疗法以前已经证明的抗炎作用，以及一项小型研究表明长期治疗停止后仍继续受益的结果，一项更大的研究正在评估其对气道重塑标志物的影响。
