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

Abstract:

: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.

journal_name

Allergy

journal_title

Allergy

authors

Rabe KF,Calhoun WJ,Smith N,Jimenez P

doi

10.1111/j.1398-9995.2011.02617.x

subject

Has Abstract

pub_date

2011-09-01 00:00:00

pages

1142-51

issue

9

eissn

0105-4538

issn

1398-9995

journal_volume

66

pub_type

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