Abstract
Acute exacerbation is the major cause of asthma morbidity, mortality, and health-care costs. Respiratory viral infections, particularly rhinovirus (RV) infections, are associated with the majority of asthma exacerbations. The risk for bronchoconstriction with RV is associated with allergic sensitization and type 2 airway inflammation. The efficacy of the humanized anti-IgE monoclonal antibody omalizumab in treating asthma and reducing the frequency and severity of RV-induced asthma exacerbation is well-known. Despite these clinical data, mechanistic details of omalizumab's effects on RV-induced asthma exacerbation have not been well-defined for years due to the lack of appropriate animal models. In this Perspective, we discuss potential IgE-dependent roles of mast cells and dendritic cells in asthma exacerbations.
Highlights
Asthma is a T helper cell 2 (Th2) cell-driven chronic inflammatory lung disease, characterized by airway inflammation, airway hyperresponsiveness (AHR), airway remodeling, and reversible airway obstruction [1, 2]
Clinical evidence supports the pathogenic role for IgE and mast cells in asthma and RV-induced asthma exacerbation: mast cells are increased in the airway epithelium [30] and within the smooth muscle layer [31,32,33] in allergic asthma, and in the alveolar parenchyma of uncontrolled allergic asthma [34]
While most studies failed to mention on the role of IgE or mast cells [64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79], a recent study showed that house dust mite (HDM)-induced airway inflammation is not dependent on IgE or FcεRI [80]
Summary
Asthma is a T helper cell 2 (Th2) cell-driven chronic inflammatory lung disease, characterized by airway inflammation, airway hyperresponsiveness (AHR), airway remodeling, and reversible airway obstruction [1, 2]. While most studies failed to mention on the role of IgE or mast cells [64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79], a recent study showed that HDM-induced airway inflammation is not dependent on IgE or FcεRI [80].
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