Eosinophils, analogous to mast cells, are leading cells of allergic inflammation. Eosinophils recruite various biomolecules; among them, IL-5 and IL-33 are the main factors required for the survival, maintenance, and activation of circulating and tissue eosinophils, preventing their apoptosis.
Eosinophils have two types of granules, primary and specific/crystalloid, which contain galectin 10, major basic protein, eosinophilic cationic protein, eosinophilic peroxidase, enzymes, cysteinyl leukotrienes, histaminase, etc. Most of these factors release during degranulation, affect parasites in a toxic manner, and participate in allergic inflammation.
Charcot-Leyden (CLC) crystals are found in many biologic fluids, including asthmatic patients' sputum, and consist of a chitinase-like protein, re-named galectin-10 (CLC protein). CLC protein (galectin-10) is overexpressed in eosinophils and identified in basophils, lymphocytes, and macrophages. Stimulating signals can trigger massive eosinophil release of galectin-10 and even induce eosinophil apoptosis or necrosis. The formation of CLCs may be used as a potential biomarker for eosinophilic inflammation.
Eosinophils are capable of phagocytosis and extracellular DNA trap (NETosis). They can take part in antibody-dependent cellular cytotoxicity (ADCC) against parasites.
Tissue infiltration by eosinophils can correlate with the severity of atopic diseases. For example, Th2-high/eosinophilic endotype in allergic asthma is sometimes a source of uncontrolled asthma.
i.e., elevated eosinophil count in the blood, may be caused by parasitic invasions, atopic allergic conditions, drug allergy, some forms of primary immunodeficiencies, an eosinophilic leukemoid reaction, eosinophilic esophagitis, and other non-allergic disorders of tissues.
Eosinophil activity is regulated by IL-5, CCL11 (Eotaxin-1), CCL24 (Eotaxin-2), CCL26 (Eotaxin-3), and other biomolecules.