Professor Philip Bardin
Severe asthmatics uncontrolled on standard treatments with long-acting beta-agonist and inhaled corticosteroids may be eligible for and responsive to biological therapies that target cytokines. The underlying pathogenesis of allergic asthma can be broadly characterized as T helper-2 (Th2) cell-mediated disease. Cytokines generated from Th2 cells including IL-4, IL-5 and IL-13 are now known to be closely associated with pathogenetic mechanisms in asthma.
Targeting the pathways involved in Th2 inflammation in asthma has been successful and eosinophils appear to be a reliable biomarker to detect patients in whom this strategy may be effective. However, a significant number of severe asthmatics (approximately 30-50%) do not have a Th2-high phenotype that will limit the use of these new therapies. More innovation is needed to develop new therapies and expand the repertoire of biomarkers to identify severe asthma phenotypes likely to respond to targeted treatments.
Centre for Innate Immunity & Infectious Diseases
Monash Lung and Sleep
Journal and article title
A blood eosinophil level of >300 cells/μL or higher is currently the most easily accessible biomarker to identify severe asthmatics who are likely to respond to biological therapies that target cytokines.
Phenotyping severe asthmatics using a combination of biomarkers may be best able to identify which patients are likely to derive benefits from targeted anti-cytokine therapy.