Eosinophilic vs. Neutrophilic Asthma

Understanding the molecular mechanisms and heterogeneity of asthma has allowed the discovery of two distinct endotypes based on the mechanisms driving the underlying airway inflammation: eosinophilic asthma, a subtype of T2-high asthma, and neutrophilic asthma, a subtype of non-T2 asthma or T2-low asthma. In this review, we highlight the current knowledge about the immunopathology of these distinct subtypes and their clinical and therapeutic implications. The intricate interplay of immune pathways has been recently evaluated in both eosinophilic and neutrophilic asthma. The delineation of signaling molecules and cytokines in the eosinophilic pathway has led to the identification of biomarkers that can guide in diagnosing and prognosticating patients and the advent of several targeted biologic therapies. However, the mechanisms of neutrophilic asthma are still not well understood and constitute an unmet need and a therapeutic challenge especially that patients with this type of asthma are often characterized by severe and refractory disease. The understanding of the heterogeneity of asthma profiles and the fundamental inflammatory pathways driving airway inflammation helped in stratifying the disease into distinct endotypes and phenotypes. Recognizing the diverseness of the disease helped in understanding the varying response to treatment options and accounting for the shift in treatment paradigms from a “one size fits all” approach to targeted personalized medicine mostly in eosinophilic asthma. Knowledge gaps exist in the understanding of the pathophysiology of neutrophilic asthma with further studies needed to elucidate its pathogenesis and to develop more effective therapy to target this subgroup of patients with more resistant disease.