Case series reports relapsing hypereosinophilia linked to Pseudomonas aeruginosa in asthma on anti-IL-5 therapy, suggesting bacterial infection can drive IL-5-independent eosinophilia.
Biologic therapies targeting IL-5 or its receptor reduce eosinophilia and exacerbations in asthma. Breakthrough eosinophilic attacks are usually considered biologic failure. We report 2 patients with severe asthma receiving mepolizumab or benralizumab who developed relapsing hypereosinophilia associated with Pseudomonas aeruginosa airway infection. Case 1 was a 71-year-old woman in Canada with severe eosinophilic asthma and COPD overlap whose eosinophils suddenly rebounded to 1,400 cells/μL during an acute exacerbation while on mepolizumab, coinciding with P aeruginosa infection and resolving after antibiotic treatment. Case 2 was a 56-year-old woman in the United Kingdom with late-onset asthma who developed marked eosinophil rebound (1,690 cells/μL) during benralizumab therapy, again associated with Paeruginosa infection and resolving after antipseudomonal therapy. These cases suggest that P aeruginosa may drive eosinophilia through IL-5-independent mechanisms. Sputum cultures should be considered during exacerbations in patients treated with anti-IL-5 or IL-5R therapies, regardless of type 2 biomarkers.
No takes yet. Share an insight, caveat, or question.
Rivard et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: