Blood Eosinophil Subtype-Specific Protein Gene Expression and Eosinophil-Derived Serum Mediators in Allergic Asthma Patients After Bronchial Challenge with Dermatophagoides pteronyssinus.

BACKGROUND: Differences in gene expression between inflammatory-like (iEOS-like) and resident-like (rEOS-like) eosinophil subtypes, and in eosinophil-derived serum mediators, may reflect eosinophil functional activity and their potential role in the pathogenesis of allergic asthma (AA). METHODS: Twenty-three patients with non-severe AA and thirteen healthy subjects (HS) were examined. AA patients underwent a bronchial allergen challenge (BAC) with Dermatophagoides pteronyssinus and were re-evaluated 24 h later. Blood eosinophils were isolated by gradient centrifugation and magnetic separation, followed by subtyping based on CD62L expression. Gene expression was assessed by TaqMan-based quantitative PCR. Serum eosinophil cationic protein (ECP), eosinophil-derived neurotoxin (EDN), Galectin-10 (Gal10), and NADPH oxidase 2 (NOX2) were measured using ELISA. RESULTS: Blood eosinophil subtypes from AA patients showed significantly higher expression of CLC, ECP, EPX, EDN, MBP, ALOX5, NOX2, and TGF-β1 compared to those from HS (p < 0.05), with no significant changes in LTA4H and LTC4S. iEOS-like cells in AA patients exhibited higher CLC and EPX expression compared to rEOS-like cells, (p < 0.05). Following BAC, CLC, MBP, and TGF-β1 expression increased in both eosinophil subtypes, while EPX and NOX2 increased only in iEOS-like cells (all p < 0.05). Serum ECP, EDN, and Gal10 concentrations were elevated in AA compared to HS and further increased after BAC (all p < 0.05); serum NOX2 remained unchanged. CONCLUSIONS: BAC induces a late-phase eosinophilic response in AA characterized by a partially eosinophil subtype-specific increase in gene expression and in circulating eosinophil-derived mediators. An increase in Gal10, observed at the CLC transcript level in eosinophils and in serum-but not in ECP or EDN-suggests the existence of mediator-specific mechanisms that regulate gene expression and extracellular release.