Type 2 inflammation associated with fixed airflow obstruction, bronchodilator responsiveness, and allergic sensitisation in mild to moderate asthma.

Type 2 (T2) inflammation drives key asthma features, including airway eosinophilia, airway inflammation, mucous hypersecretion, and hyperresponsiveness. Elevated T2 biomarkers, such as blood eosinophils (BEC) and FeNO are associated with exacerbations, bronchodilator responsiveness, and lung function decline. However, its impact over time on fixed airflow obstruction and allergic sensitisation in more mild controlled disease, remains less well characterised. This study examines T2 inflammation in a cross-sectional asthma cohort prior to enrolment in the MAPLE longitudinal study. T2-high GINA 1-3 patients (BEC ≥300µL or FeNO ≥ 50ppb, n=94) were compared with T2-low for clinical characteristics, flares/exacerbations, spirometry, FOT, methacholine responsiveness, bronchodilator responsiveness, AIRQ/ACQ, and allergic sensitisation. The cohort (median age 28, BMI 26, 41% female, no current smokers) included 27% in GINA step 1, 24% step 2, 48% step 3 and 12% had poor control (ACQ-6≥1.5). T2-high was identified in 49 (38%) patients and associated with lower FEV1/FVC (p<0.01), greater bronchodilator responsiveness (p<0.05, prevalence p<0.05), and higher prevalence of House Dust Mite sensitisation (p<0.05). In contrast, T2 inflammation was not associated with FOT, FEV1, AIRQ/ACQ scores. The findings suggest that in mild and more controlled asthma, T2 inflammation is associated with airflow obstruction, bronchodilator responsiveness, and allergic sensitisation, but not small airway dysfunction or symptom burden. Further insights into disease progression and stability of endotypes will be gained from the MAPLE longitudinal study.