Anti-IgE treatment, airway inflammation and remodelling in severe allergic asthma: current knowledge and future perspectives

Abstract

Asthma is a disorder of the airways involving various inflammatory cells and mediators and characterised by bronchial hyperresponsiveness, chronic inflammation and structural alterations in the airways, also known as remodelling. IgE is an important mediator of allergic reactions and has a central role in allergic asthma pathophysiology, as it is implicated in both the early and late phase allergic response. Moreover, clinical and mechanistic evidence has lately emerged, implicating IgE in the development of airway remodelling. The use of monoclonal antibodies targeting IgE, such as omalizumab, has proven very effective in improving respiratory symptoms and quality of life, while reducing asthma exacerbations, emergency room visits and the use of systemic corticosteroids in allergic severe asthma. These effects are believed to be mainly mediated by omalizumab's inhibitory effect on the initiation and further propagation of the allergic inflammation cascade. However, there is evidence to suggest that anti-IgE treatment remains effective long after it has been discontinued. In part, these findings could be attributed to the possible ameliorating effects of anti-IgE treatment on airway remodelling. In this review, we discuss recent findings supporting the notion that anti-IgE treatment modulates the complex immune responses that manifest clinically as asthma and ameliorates airway remodelling changes often observed in allergic severe asthma phenotypes.

FIGURE 1

Microphotographs (×20) of endobronchial biopsies from a) healthy control, b) mildly asthmatic and c) severe asthmatic airways demonstrating increased thickness of the basement membrane (haematoxylin–eosin stain) and goblet cell (GC) hyperplasia (periodic acid–Schiff stain) as asthma severity increases. EP: epithelium; RBMt: reticular basement membrane; Ang: angiogenesis. Scale bars=50 μm.