IgE expression pattern in lung: Relation to systemic IgE and asthma phenotypes

Background IgE-mediated responses contribute to allergy and asthma. Little is understood regarding the relationship of tissue IgE to systemic IgE, inflammation or clinical outcomes. Objectives To evaluate local IgE expression and cellular inflammation in the proximal and distal lung of normal subjects and subjects with asthma of varying severity and relate those tissue parameters to systemic IgE levels, atopy, lung function, and history of severe exacerbations of asthma. Methods Tissue from more than 90 subjects with eosinophilic (SAeo+ ) and noneosinophilic (SAeo− ) severe asthma, mild asthma and normal subjects were immunostained for IgE, signal-amplifying isoform of IgE receptor (FcεRIβ) and markers of mast cells, eosinophils, and lymphocytes. Tissue expression of IgE, FcεRIβ, cellular inflammation, serum IgE, and atopy were compared. Regression models were used to determine the relationship of local and systemic IgE to lung function and severe exacerbations of asthma. Results Mast cell–bound IgE was present along airways but absent in lung parenchyma. Although the groups were similar in systemic/serum IgE and atopy, local/tissue IgE was highest in SAeo+ and correlated with eosinophils and lymphocytes ( rs = 0.52, P < .0001; and rs = 0.23, P = .03, respectively). Higher local IgE was associated with better lung function, but also with more severe exacerbations of asthma. Conclusion Local IgE appears to be primarily a component of responses within the mucosal immune compartment and is related to cellular inflammation, lung function, and clinical outcomes in asthma. Clinical implications Local/airway IgE-related processes rather than systemic markers of atopy may be relevant in determining clinical outcomes in asthma.