Airway eosinophilic inflammation is a central feature in asthma which is mainly driven by type 2 response. The expression of galectin-13 was up-regulated in a parasitic infection model which is also characterized by type 2 immune response. We hypothesized that galectin-13 may be involved in airway eosinophilic inflammation in asthma.
To unveil the role of galectin-13 in asthma airway inflammation.
We measured galectin-13 expressions in bronchial brushings, sputum, serum of asthma patients (n =54) and healthy controls (n =15), analyzed the correlations between galectin-13 expression and airway eosinophilia. We use human bronchial epithelial (HBE) cells to investigate the possible mechanism by which galectin-13 participates in eosinophilic inflammation.
The expression of galectin-13 was markedly increased in subjects with asthma compared to control. Epithelial galectin-13 mRNA levels in asthmatic subjects were strongly correlated with eosinophilic airway inflammation (the percentage of sputum eosinophils, the number of eosinophils in bronchial submucosa, and FeNO) and Th2 signature genes (CLCA1, POSTN and SERPINB2). Inhaled corticosteroid (ICS) treatment reduced galectin-13 expression, and plasma galectin-13 level reflects airway response to asthma therapy. In cultured human bronchial epithelial cells, knockdown of galectin-13 suppressed IL-13-stimulated MCP-1 and eotaxin-1 by inhibiting the activation of EGFR and ERK.
Galectin-13 is a novel marker for airway eosinophilia in asthma, and may contribute to allergic airway eosinophilic inflammation by regulating the expression of MCP-1 and eotaxin-1. Plasma galectin-13 level may be useful for predicting responses to asthma therapy.

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