Nasal eosinophilia as a noninvasive biomarker of type 2 inflammation and treatment response in children with asthma

Objective The dominant paediatric asthma endotype is type 2 inflammation with eosinophilic airway infiltration. In routine clinical practice, the assessment of eosinophilic airway inflammation is limited by the availability and feasibility of invasive or semi-invasive diagnostic methods, which are technically demanding and ethically challenging in children. Surrogate biomarkers including peripheral blood eosinophil counts or serum IgE do not always reliably reflect local airway inflammation. Nasal cytology is widely used in rhinoallergology and may extend to asthma under the unified airway hypothesis. This retrospective study evaluated its applicability as a non-invasive marker of local eosinophilic inflammation and analysed the effect of different therapeutic approaches on nasal eosinophil proportions in children with asthma.Methods A total of 202 children aged 7–18 years were included in the study and stratified according to the treatment type and fractional exhaled nitric oxide (FeNO) values. Absolute peripheral blood eosinophil counts, nasal eosinophil percentages, FeNO levels and age were assessed.Results Antihistamines and leukotriene receptor antagonists were associated with a significant reduction in nasal eosinophilia (p = 0.004 and p = 0.001, respectively), whereas inhaled corticosteroids showed no significant effect (p = 0.928). A significant positive association was demonstrated between FeNO levels and nasal eosinophilia (p < 0.001), while age showed a significant negative effect (p < 0.001).Conclusion Nasal cytology may represent an easily applicable, and ethically acceptable tool for non-invasive monitoring local eosinophilic inflammation in paediatric asthma. Nasal eosinophilia appears to reflect dynamic airway inflammatory changes more directly than peripheral blood eosinophils and may be useful adjunctive marker for monitoring treatment-related changes and guiding personalized therapy.