Gene profiles differ in adult- and childhood-onset severe asthma
medwireNews: A European study suggests gene profiles differ in severe asthma that begins in adulthood rather than childhood, indicating distinct underlying mechanisms at work.
Inflammatory pathways involving eosinophils, mast cells, and group 3 innate lymphoid cells (ILC3s) characterized adult-onset severe asthma, report the researchers.
They suggest in the Journal of Allergy and Clinical Immunologythat these pathways “could represent useful targets for the treatment of adult-onset severe asthma.”
The team studied information collected at baseline visits among adult patients with severe asthma at 16 clinical centers in 11 European countries taking part in the Unbiased Biomarkers for the Prediction of Respiratory Disease Outcomes (U-BIOPRED) study.
The study included patients with a confirmed diagnosis of asthma and either uncontrolled disease despite treatment with high-dose inhalation medication and a second controller or the need for systemic oral corticosteroids or omalizumab to achieve asthma control, regardless of smoking history.
Of the 421 patients with severe asthma in the U-BIOPRED cohort, 253 (60.1%) had their first asthma diagnosis or onset of symptoms when they were aged 18 years or older and were identified with adult-onset disease, whereas for 158 (37.5%) this had occurred when they were younger.
Gene expression was assessed using total RNA from all available samples from nasal brushings (n=41), induced sputum (n=83), endobronchial brushings (n=65), or endobronchial biopsies (n=47).
Pieter-Paul Hekking (Academic Medical Center, Amsterdam, the Netherlands) and co-workers report significantly different enriched gene signatures in patients with adult-onset versus childhood-onset severe asthma.
Five such gene signatures were identified in nasal brushings, three in sputum, and six in endobronchial brushings. These signatures included those associated with response to fluticasone treatment, with house dust mite-induced asthma, and those associated with eosinophilia, mast cells, and macrophages, as well as with ILC3s.
“These gene signatures suggest that multiple underlying pathways play a role in adult-onset severe asthma,” say the researchers.
One gene signature associated with induced lung injury was more enriched in patients with adult-onset severe asthma compared with childhood-onset disease, whereas another was less so.
Hekking et al conclude that adult-onset severe asthma has “complex underlying pathways involving eosinophils, ILC3s and mast cells.”
They believe: “These point towards possible new targets that could represent targeted treatments for subgroups of adult-onset severe asthma.”
By Anita Chakraverty
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