Galectin-10 is a member of the lectin family and one of the most abundant cytoplasmic proteins in human eosinophils. Except for some myeloid leukemia cells, basophils, and minor T cell populations, galectin-10 is exclusively present in eosinophils in the human body. Galectin-10 forms Charcot–Leyden crystals, which are observed in various eosinophilic diseases. Accumulating studies have indicated that galectin-10 acts as a new biomarker for disease activity, diagnosis, and treatment effectiveness in asthma, eosinophilic esophagitis, rhinitis, sinusitis, atopic dermatitis, and eosinophilic granulomatosis with polyangiitis. The extracellular release of galectin-10 is not mediated through conventional secretory processes (piecemeal degranulation or exocytosis), but rather by extracellular trap cell death (ETosis), which is an active cell death program. Eosinophils undergoing ETosis rapidly disintegrate their plasma membranes to release the majority of galectin-10. Therefore, elevated galectin-10 levels in serum and tissue suggest a high degree of eosinophil ETosis. To date, several studies have shown that galectin-10/Charcot–Leyden crystals are more than just markers for eosinophilic inflammation, but play functional roles in immunity. In this review, we focus on the close relationship between eosinophils and galectin-10, highlighting this protein as a potential new biomarker in eosinophilic diseases.
Uncontrolled airway mucus is associated with diverse diseases. We hypothesized that the physical characteristics of infiltrating granulocytes themselves affect the clinical properties of mucus. Surgically obtained nasal mucus from patients with eosinophilic chronic rhinosinusitis (ECRS) and neutrophil-dominant non-eosinophilic chronic rhinosinusitis (non-ECRS) was assessed in terms of computed tomography (CT) density, viscosity, water content, wettability, and granulocyte-specific proteins. In an observational study, we found that nasal mucus from patients with ECRS had significantly higher CT density, viscosity, dry weight, and hydrophobicity than mucus from patients with non-ECRS. The levels of eosinophil-specific proteins in nasal mucus correlated with its physical properties. When isolated human eosinophils and neutrophils were stimulated to induce extracellular traps followed by aggregate formation, we found that cell aggregates showed physical and pathological findings that closely resembled mucus. Co-treatment with heparin (which slenderizes the structure of eosinophil extracellular traps) and DNase efficiently induced a reduction in the viscosity and hydrophobicity of both eosinophil aggregates and eosinophilic mucus. The present study highlights the pathogenesis of mucus stasis in infiltrated granulocyte aggregates from a new perspective. The combination of DNase and heparin might be a novel therapeutic modality against pathologic viscous eosinophilic mucus.
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