嗜酸性粒细胞调控网络在ECRS发生发展中的机制研究OA

Eosinophilic chronic rhinosinusitis(ECRS)is a refractory nasal inflammatory disease characterized by a Th2-type inflammatory response,high heterogeneity,and high recurrence rate.Eosinophils play a central role in the pathological process of ECRS,and their abnormal differentiation,maturation,and functional alterations are the key factors for the occurrence and development of ECRS.In the bone marrow,interleukin(IL)-5 mediates the"transit amplification"of eosinophil progenitor cells through the JAK-STAT signaling axis,which is a critical determinant of the number of peripheral blood eosinophils.The CCAAT/enhancer binding protein(C/EBP)family and GATA transcription factors coordinately and antagonistically regulate eosinophil lineage commitment.During peripheral recruitment,IL-5 promotes the migration of eosinophils across the endothelium by activating β2 integrins,while chemokines are the primary pathways directing their migration to the nasal mucosa.In the local nasal mucosa of ECRS,type 2 innate lymphoid cells(ILC2s)and Th2 cells form a positive feedback loop to release IL-5.It not only the survival of eosinophils by blocking 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 the differentiation and maturation of the eosinophilic cell lineage in the bone marrow,the peripheral recruitment,and the local activation in the nasal cavity.It also explores the role of the network in the pathogenesis of ECRS.The aim is to provide a theoretical basis for the search for new therapeutic targets for ECRS in clinical practice.