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

• Published in: Allergy (Copenhagen) 2011-09, Vol.66 (9), p.1142-1151
• Main Authors: Rabe, K. F., Calhoun, W. J., Smith, N., Jimenez, P.
• Format: Article
• Language: English
• Subjects: airway remodeling; Airway Remodeling - drug effects; allergic asthma; Animals; Antibodies, Anti-Idiotypic - adverse effects; Antibodies, Anti-Idiotypic - therapeutic use; anti‐IgE; Asthma; Asthma - drug therapy; Asthma - immunology; Asthma - pathology; Biological and medical sciences; Chronic obstructive pulmonary disease, asthma; Dendritic cells; Dermatology; Drug therapy; Eosinophilia; Epithelium; Fc receptors; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Granulocyte-macrophage colony-stimulating factor; Humans; Hypersensitivity; Hypersensitivity - immunology; Immunoglobulin E; Immunoglobulins; Inflammation; Interleukin 13; Interleukin 4; Interleukin 5; Leukocytes (basophilic); Mast cells; Medical sciences; Monoclonal antibodies; omalizumab; Pneumology; Respiratory tract; Respiratory tract diseases; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis; Smooth muscle
• ISSN: 0105-4538; 1398-9995
• DOI: 10.1111/j.1398-9995.2011.02617.x

To cite this article: Rabe KF, Calhoun WJ, Smith N, Jimenez P. Can anti‐IgE therapy prevent airway remodeling in allergic asthma? Allergy 2011; 66: 1142–1151. 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.