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Clinical phenotypes in both adult and pediatric asthma have been determined using supervised definition-driven classification and unsupervised data-driven clustering methods. Efforts to understand the underlying inflammatory patterns of severe asthma have led to the seminal discovery of type 2-high versus type 2-low phenotypes and to the development of biologics targeted at type 2-high inflammation to reduce the rates of severe asthma exacerbations. Type 2-high asthma is characterized by upregulation of T helper 2 immune pathways including interleukin (IL)-4, IL-5, and IL-13 along with eosinophilic airway inflammation, sometimes allergic sensitization, and responsiveness to treatment with corticosteroids. Type 2-low asthma is poorly responsive to corticosteroids and is not as well characterized as type 2-high asthma. Type 2-low asthma is limited by being defined as the absence of type 2-high inflammatory markers. Choosing a biologic for the treatment of severe asthma involves the evaluation of a panel of biomarkers such as blood eosinophils, total and specific immunoglobulin E\/allergic sensitization, and fractional exhaled nitric oxide. In this review, we focus on the underlying pathobiology of adult and pediatric asthma, discuss the different phenotype-based treatment options for adult and pediatric type 2-high with or without allergic asthma and type 2-low asthma, and describe a clinical phenotyping approach to patients to guide out-patient therapy. Finally, we end with a discussion of whether pediatric asthma exacerbations necessitating admission to an ICU constitute their own high-risk phenotype and\/or whether it is a part of other previously defined high-risk subgroups such as difficult-to-control asthma, exacerbation-prone asthma, and severe treatment-resistant asthma.<\/jats:p>","DOI":"10.1089\/respcare.12352","type":"journal-article","created":{"date-parts":[[2025,2,27]],"date-time":"2025-02-27T10:08:00Z","timestamp":1740650880000},"page":"649-674","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":22,"title":["Asthma Phenotypes and Biomarkers"],"prefix":"10.1177","volume":"70","author":[{"given":"Jocelyn R.","family":"Grunwell","sequence":"first","affiliation":[{"name":"Dr. Grunwell is affiliated with Division of Critical Care Medicine, Department of Pediatrics, Children\u2019s Healthcare of Atlanta, Emory University School of Medicine, Atlanta, Georgia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne M.","family":"Fitzpatrick","sequence":"additional","affiliation":[{"name":"Dr. Fitzpatrick is affiliated with Division of Pulmonary, Allergy\/Immunology, Cystic Fibrosis, and Sleep Medicine, Department of Pediatrics, Children\u2019s Healthcare of Atlanta, Emory University School of Medicine, Atlanta, Georgia."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2025,2,10]]},"reference":[{"key":"e_1_3_3_2_2","unstructured":"Centers for Disease Control and Prevention\/National Center for Health Statistics. 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