Eosinophils, bone marrow-derived granulocytes, modulate the function of structural cells and immunocytes and play critical roles in host defense against virus and bacteria, in the homeostasis of innate and adaptive immunity, and in tissue and vascular remodeling. Dysregulated eosinophilia, however, evokes pathology such as asthma, nasal polyps, vasculitis, and atopic dermatitis [
33,
34]. Using bronchial biopsies, investigators showed that numbers of inflammatory cells including eosinophils were elevated in subjects with atopic asthma when compared with those who were non-atopic or healthy [
35]. Others determined that severe persistent asthma subjects could be divided into those with or without airway tissue eosinophils [
36]. Importantly, therapeutic strategies that decreased sputum eosinophil levels, a surrogate of airway eosinophilia, markedly improved pulmonary function and exacerbation rates in comparison to subjects who were treated by guidelines alone. Unfortunately, accessibility to testing sputum or tissue eosinophil levels remains reserved for research purposes and requires substantial expertise. Accordingly, investigators have extensively studied the validity and reliability of blood eosinophil levels as a biomarker of disease onset and severity [
31]. Using monoclonal antibodies, recent studies show that targeting IL-5, an important survival factor for eosinophils, decreased blood eosinophil counts that were associated with markedly improved exacerbation rates, patient reported outcomes and pulmonary function as compared with subjects treated with standard care [
27,
32]. Unfortunately, limitations exist in using blood eosinophil counts as severe asthma biomarkers that include: diurnal variations in blood eosinophil levels, sensitivity to systemic glucocorticoids, and lack of concordance between sputum and blood levels [
31,
37]. These limitations suggested that blood eosinophil counts should serve as supplemental biomarkers [
31].