众所周知，以嗜酸性粒细胞浸润为主的鼻息肉患者术后容易复发，治疗效果不佳。近来研究表明：上皮细胞来源的细胞因子IL-33与受体ST2结合参与巨噬细胞的极化，极化的2型巨噬细胞则促进和调节Th2型免疫反应。而我们前期的研究发现：IL-33受体ST2在鼻息肉的巨噬细胞中表达明显升高，尤其是在嗜酸性粒细胞浸润为主的鼻息肉中还存在有大量的2型巨噬细胞浸润。因此，我们推断鼻息肉上皮细胞分泌的IL-33与黏膜下巨噬细胞受体ST2结合，促进巨噬细胞极化，从而参与鼻息肉Th2型炎症的发生发展。本课题将以此为假设，利用体内外实验证明上皮细胞/IL-33-ST2/巨噬细胞-Th2型炎症通路在鼻息肉发生发展中的重要作用，以期从上皮细胞/固有免疫细胞的角度来深入探讨鼻息肉发生发展的病理机制，从而揭示鼻息肉Th2型炎症调控的机理并为其治疗提供新的靶点。

Nasal polyps with dominant esinophils infiltration were characterized by high recurrence rate and poor outcome. Recent studies have shown that IL-33, a cytokine derived from epithelial cell, can bind to the receptor ST2 to participate in the polarization of macrophages, while polarized M2 can promote and regulate Th2-type inflammation. Moreover, our initial study found that ST2 was significantly expressed in macrophages (Mφ) of nasal polyps, especially in type 2 macrophages (Mφ2) that were enriched in nasal polyps with dominant esinophils infitration. Therefore, we supposed that IL-33, derived from nasal epithelial cells, could bind the receptor ST2 on the macrophages to induce their polarization and activation, and then result in Th2-type inflammation in nasal polyps. Accordingly, the current project would verify above hypothesis by in vitro and vivo experiments, and demonstrate the important role of epithelia/IL-33-ST2/Mφ pathway in the development of nasal polyps. The purpose of this project is to explore the possible pathogenesis of nasal polyps from the connection between epithelial cells and innate immune cells, and reveal a novel possible mechanism of TH2-type inflammation in nasal polyps, which would provide a new target for the treatment of nasal polyps.