金黄色葡萄球菌与鼻息肉的发病机制密切相关。我们前期已发现IFN-λ1在鼻息肉组织中未能通过巨噬细胞发挥抗菌作用，而息肉组织内具有免疫抑制作用的M2型巨噬细胞较正常组织明显增多，表明M2型巨噬细胞与细菌的持续存在密切相关。金葡菌形成的生物膜对抗生素有很强的抗性，也能促进M2型巨噬细胞的分化，进一步妨碍细菌清除。如何加强细菌清除，抑制黏膜慢性炎症是现阶段鼻科研究亟待解决的问题。本课题拟在息肉组织内，通过流式细胞术研究金葡菌感染过程中髓源抑制性细胞（MDSCs）与巨噬细胞M2样极化的关系，体外刺激实验探寻影响细胞分化的因素，采用蛋白芯片技术筛选关键信号通路，结合MDSCs和巨噬细胞RNA-seq结果，确定MDSCs分化成M2型巨噬细胞的机制。本课题可阐明鼻息肉组织内金葡菌免疫逃逸的相关机制，针对性减少M2型巨噬细胞分化，增强细菌清除，为有效缓解鼻部慢性炎症奠定理论基础，开启鼻息肉临床治疗新思路。

Staphylococcus aureus (S. aureus) is associated with the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP). Our previous data declared that IFN-λ1 exerted its anti-bacterial role via macrophage in healthy controls, not in CRSwNP tissue. Alternative activated macrophages (M2) with immunoregulatory function were reportedly up-regulated in CRSwNP tissue compared to controls, suggesting that the persistence of S. aureus in CRSwNP tissue is related to the impaired role of macrophages. Furthermore, the formation of S. aureus biofilms are capable of subverting immune mediated bacterial clearance. Till now, effective ways to eradicate bacteria to alleviate chronic inflammations in CRSwNP are still unavailable. Here, we will investigate the relationship between myeloid derived suppressor cells (MDSCs) and the differentiation of M2 cells in CRSwNP tissue during S. aureus infection by flow cytometry. The ex vivo model will be used to analyze factors affecting the differentiation of M2 cells from MDSCs. The underlying pathways of the differentiation of M2 cell from MDSCs will be confirmed via the combination of pathway screening by the Proteome array and RNA-seq results of macrophages and MDSCs. This project will declare the resource of M2 cells during S. aureus infection. We expect to develop new strategies to inactive or reduce M2 cell and enhance the phagocytosis of macrophage, which provides theoretical evidence for chronic inflammation alleviation and enlarges the treatments of CRSwNP.