Type-2 airway inflammation in mild asthma patients with high blood eosinophils and high fractional exhaled nitric oxide.

Type-2 (T2) inflammation is a characteristic feature of asthma. Biological therapies have been developed to target T2-inflammation in asthma. IL-13 is a key component of T2-inflammation in asthma, driving mucus hypersecretion, IgE-induction and smooth muscle contraction. Early phase clinical trials for treatments that target T2-inflammation require biomarkers to assess pharmacological effects. The aim of this study was to examine levels of IL-13 inducible biomarkers in the airway epithelium of mild asthma patients compared to healthy controls.
Ten mild asthma patients with high blood eosinophil and high fractional exhaled nitric oxide (FeNO) were recruited, and six healthy subjects. Blood eosinophil and FeNO reproducibility was assessed prior to bronchoscopy. Epithelial brushings were collected and assessed for IL-13 inducible gene expression.
Blood eosinophil and FeNO levels remained consistent in both asthma patients and healthy subjects. Of the 11 genes assessed, expression levels of 15LOX1, POSTN, CLCA1, SERPINB2, CCL26 and NOS2 were significantly higher in asthma patients compared to healthy controls. These 6 genes, present in mild asthma patients with T2 inflammation, have the potential to be used in translational early phase asthma clinical trials of novel therapies as bronchial epithelial biomarkers.