IL-25具有重要的促进气道重塑的致病作用，我们新近报道了在鼻息肉（NP）中IL-25水平和上皮重塑、组织嗜酸性粒细胞（EOS）炎症显著相关，但IL-25促进NP上皮重塑的细胞-分子机制仍不清。我们预实验发现IL-25并不能直接促进鼻粘膜上皮细胞增殖，而是具有促进EOS向促炎致病表型转化，并增强EOS促上皮重塑功能的作用。据此我们推测：IL-25是通过驱动EOS促进NP上皮重塑的发病。为了验证此假设，我们拟通过分离人EOS和鼻上皮细胞，建立体外EOS和上皮细胞ALI共培养模型，采用体外干预和阻断实验，进一步明确IL-25驱动EOS对上皮重塑的促进作用和介导此病理过程的分子机制，本研究将有助于阐明IL-25在NP发病中的重要致病作用和机制，为以IL-25为干预靶标的精准治疗提供新的实验和理论基础。

IL-25 plays important pathogenic roles in promoting airway remodeling. We have recently reported that IL-25 levels in nasal polyps (NP) are significantly associated with epithelial remodeling and tissue eosinophil (EOS) inflammation. However, the cell-molecular mechanism underlying IL-25 promotes NP epithelial remodeling remains unclear. We preliminarily found that IL-25 did not directly promote the proliferation of nasal epithelial cells, but promoted EOS to acquire a pro-inflammatory pathogenic phenotype with an enhanced potential in promoting epithelial remodeling. Therefore, we speculate that IL-25 promotes NP epithelial remodeling by driving the pathogenic function of EOS. To address this hypothesis, we intend to isolate human EOS and primary nasal epithelial cells and establish a co-culture model of EOS and epithelial cells in vitro. Using in-vitro blocking experiments to determine the effect of IL-25-driven EOS on epithelial remodeling, as well as the underlying molecular mechanism. This study will elucidate the important pathogenic role of IL-25 in the pathogenesis of NP and provide new evidence and rationale for the precise targeting of IL-25.