LAUSR

The diversity in pathophysiological, immunological and clinical patterns seen in asthma patients was the key driver for a wealth of biomarker studies during the past decades. Early on, asthma was divided into allergic and non-allergic disease. It was the use of cluster analysis approaches that further increased our understanding of the variety of clinical asthma phenotypes. Several variables were identified to be important to classify patients into clusters, such as the patients’ age of onset, body mass index (BMI), allergy status and sputum eosinophil levels [1, 2]. On a cellular level, four phenotypes based on the levels of sputum granulocytes were defined: eosinophilic, non-eosinophilic, mixed granulocytic and paucigranulocytic asthma (figure 1) [3]. It is increasingly evident that the airway inflammatory environment in patients with asthma is the result of a spectrum of immune responses rather than a dichotomy of T2 or non-T2 inflammation, where multiple pathways may be active. https://bit.ly/3vodoSS