Gal-10, the predominant component of Charcot-Leyden Crystals (CLCs), is a glycoprotein of the lectin family produced by eosinophils, basophils and T cells, that auto-crystallizes upon activation and cytolysis of eosinophils. In asthma, CLCs formation promotes tissue damage and pro-inflammatory Th1 and Th2 cytokines.

The study aimed to investigate airway levels of Gal-10, together with IL-5, IFN?, and MUC-5AC, in the nasal lavage (NL) fluid of children with SAR. Furthermore, we evaluated the role of Gal-10 in nasal epithelium remodeling using a three-dimensional (3D) ex vivo outgrowth model of nasal respiratory mucosa. Gal-10, IL-5, IFN? and MUC-5AC levels were assessed by ELISA in NL of 32 patients with SAR. 3D outgrowths were cultured for 21 days and stimulated with or without selected NL samples (20%) with high levels of Gal-10 and subsequently embedded in paraffin for immunohistochemical evaluation of E-cadherin and Vimentin.

The results obtained by ELISA showed that NL levels of Gal-10 correlated with IL-5 (?=0.6; p<0.001) and MUC-5AC (?=0.7; p<0.001) concentrations, and inversely correlated with INF? (?=-0.65; p=0.007). Preliminary results obtained in 3D outgrowths showed an increased expression of the Vimentin mesenchymal marker in samples stimulated with NL containing higher levels of Gal10, whilst no differences were detected in E-cadherin expression.

These findings suggest, overall, the potential involvement of Gal-10 in promoting Th-2 type inflammation and mucus overproduction in the NL of children with SAR. Furthermore, our results might indicate a role of Gal-10 in driving nasal epithelium remodeling and de-differentiation.