Eosinophilic chronic rhinosinusitis (ECRS) is a refractory inflammatory disease of the nasal cavity characterized by Type 2 inflammation, with strong heterogeneity and a high recurrence rate. Eosinophils play a central role in its pathology, and their abnormal differentiation, maturation, and functional alterations are key to the pathogenesis and progression of ECRS. In the bone marrow, IL-5 mediates the "transit amplification" of eosinophil progenitor cells through the JAK-STAT signaling axis, serving as a critical determinant of peripheral blood eosinophil counts. The C/EBP family and GATA transcription factors coordinately and antagonistically regulate eosinophil lineage commitment. During peripheral recruitment, IL-5 promotes eosinophil transmigration across the endothelium by activating β2 integrins, while chemokines are the primary pathways directing their migration to the nasal mucosa. Locally, within the ECRS nasal mucosa, type 2 innate lymphoid cells (ILC2s) and Th2 cells form a positive feedback loop, releasing IL-5. This not only prolongs eosinophil survival by inhibiting Bid but also activates the release of granule proteins and other products, exacerbating tissue remodeling and inflammatory injury. This review systematically summarizes the regulatory networks governing eosinophil lineage commitment, bone marrow differentiation and maturation, peripheral recruitment, and local activation within the nasal cavity. It also explores the role of this network in the pathogenesis of ECRS, aiming to provide a theoretical basis for identifying novel therapeutic targets for ECRS.