The term “eosinophilic” asthma (EA) generally refers to the clinical inflammatory phenotype of asthma wherein a significant number of sputum, airway, and/or blood eosinophils are present. Conversely, individuals with “noneosinophilic” asthma (NEA) may still demonstrate low numbers of eosinophils, but the dominant inflammatory cell type may include neutrophils, mixed granulocyte inflammatory cells, or very few inflammatory cells, termed paucigranulocytic inflammation. Although the mechanisms driving EA are becoming clearer, by contrast much less attention has been given to the underlying mechanisms that drive NEA, leading to a lack of available therapies for this patient population.

Although “phenotype” refers to the observable characteristics of disease in an individual, by “endotypes” we mean the specific biological mechanism that causes those observed properties of any given phenotype. Understanding the manifold mechanisms or endotypes contributing to EA and NEA and the resulting clinical phenotypes derived from these endotypes will lead to novel treatment options and provide an opportunity for more precise and tailored treatments. This review highlights the mechanisms currently believed to underlie the recognized subphenotypes of EA and NEA and briefly discusses their clinical presentations as well as implications for treatment.