Michael C Peters1,2,3, Michelle-Linh T Nguyen4, Eleanor M Dunican5,6,7. 1. The Airway Clinical Research Center, University of California, Box 0130, 505 Parnassus Avenue, San Francisco, CA, 94143, USA. Michael.peters@ucsf.edu. 2. Division of Pulmonary and Critical Care Medicine, University of California, Box 0130, 505 Parnassus Avenue, San Francisco, CA, 94143, USA. Michael.peters@ucsf.edu. 3. Cardiovascular Research Institute, University of California, Box 0130, 505 Parnassus Avenue, San Francisco, CA, 94143, USA. Michael.peters@ucsf.edu. 4. Stanford University School of Medicine, Stanford, CA, 94305, USA. 5. The Airway Clinical Research Center, University of California, Box 0130, 505 Parnassus Avenue, San Francisco, CA, 94143, USA. 6. Division of Pulmonary and Critical Care Medicine, University of California, Box 0130, 505 Parnassus Avenue, San Francisco, CA, 94143, USA. 7. Cardiovascular Research Institute, University of California, Box 0130, 505 Parnassus Avenue, San Francisco, CA, 94143, USA.
Abstract
PURPOSE OF REVIEW: Over the past decade, the most important advance in the field of asthma has been the widespread recognition that asthma is a heterogeneous disease driven by multiple molecular processes. RECENT FINDINGS: The most well-established molecular mechanism in asthma is increased airway type-2 inflammation, and consequently, non-invasive biomarkers of increased airway type-2 inflammation, such as blood eosinophil counts or blood periostin levels, have proven important in stratifying asthma patients in clinical trials of type-2 cytokine inhibitors. However, it remains ambiguous how well these non-invasive biomarkers represent airway measures of type-2 inflammation in asthma. As a result, the utility of these biomarkers to assist with asthma management or as research tools to better understand asthma pathogenesis remains unclear. This article reviews primary data assessing biomarkers of airway type-2 inflammation in asthma and describes how the use of biomarkers can advance a precision medicine approach to asthma treatment.
PURPOSE OF REVIEW: Over the past decade, the most important advance in the field of asthma has been the widespread recognition that asthma is a heterogeneous disease driven by multiple molecular processes. RECENT FINDINGS: The most well-established molecular mechanism in asthma is increased airway type-2 inflammation, and consequently, non-invasive biomarkers of increased airway type-2 inflammation, such as blood eosinophil counts or blood periostin levels, have proven important in stratifying asthmapatients in clinical trials of type-2 cytokine inhibitors. However, it remains ambiguous how well these non-invasive biomarkers represent airway measures of type-2 inflammation in asthma. As a result, the utility of these biomarkers to assist with asthma management or as research tools to better understand asthma pathogenesis remains unclear. This article reviews primary data assessing biomarkers of airway type-2 inflammation in asthma and describes how the use of biomarkers can advance a precision medicine approach to asthma treatment.
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