Type 2 innate lymphoid cells: A novel biomarker of eosinophilic airway inflammation in patients with mild to moderate asthma

Abstract

BackgroundEosinophilic airway inflammation can predict the exacerbation of asthma, and we can improve the management of asthma by monitoring the eosinophilic airway inflammation. Although induced sputum and sputum eosinophil count is the gold standard test for diagnosing eosinophilic asthma, a more accessible and receptive method is needed for clinical practice. Type 2 innate lymphoid cells (ILC2) have recently been proposed to play a crucial role in eosinophilic inflammation and have been identified in peripheral blood from patients with asthma. ObjectivesWe sought to identify simple and feasible biomarkers which can predict eosinophilic airway inflammation in asthmatic patients. MethodsSputum was induced for the assessment of eosinophils in 150 asthmatic patients. In parallel, the proportion of ILC2s of peripheral blood lymphocytes (%ILC2), blood eosinophil counts, total immunoglobulin E (IgE), fractional exhaled nitric oxide (FeNO) and lung function tests were measured. 42 healthy donors served as controls. Results126 patients finished sputum induction and produced adequate sputum. The ILC2 level was significantly increased in eosinophilic asthmatic patients compared with non-eosinophilic asthmatic patients (0.117 ± 0.090versus0.035 ± 0.021, p < 0.001). A multiple regression model, including age, sex, BMI, blood eosinophil counts, FeNO, IgE and %ILC2, showed that %ILC2, blood eosinophil counts and FeNO were correlative factors of sputum eosinophil counts (p < 0.001, p = 0.037, p < 0.001, respectively) and %ILC2 was the most significant subset of airway eosinophilic inflammation (Estimate = 11.385). A receiver operating characteristic (ROC) analysis showed a sensitivity of 67.7% and a specificity of 95.3% for %ILC2 of 0.076 to distinguish eosinophilic asthmatic patients from non-eosinophilic asthmatic patients. ConclusionILC2 is a surrogate marker of airway eosinophilic inflammation in patients with mild to moderate asthma and has great potential advantages for selecting the asthmatic patients most likely to benefit from therapeutics targeting Th2 inflammation.