细菌和病毒在慢性鼻窦炎伴鼻息肉（CRSwNP）发病机制中发挥重要作用，拮抗鼻部细菌和病毒是抑制黏膜慢性炎症的有效途径。IFN-λ在呼吸道有抗病毒活性，研究鼻黏膜IFN-λ调节细菌感染的作用，期望能同时有效控制细菌病毒感染，为治疗CRSwNP提供新方向。本课题前期建立鼻黏膜金葡菌体外感染模型，在此基础上发现金葡菌诱导IFN-λ产生。拟通过组织内金葡菌定量确定IFN-λ是否抑制细菌增殖，进而从组织机械屏障和固有免疫细胞两方面评估IFN-λ对上皮紧密连接、黏蛋白、抗菌肽和巨噬细胞的影响，探索IFN-λ调节细菌感染的机制。最后采用IFN-λ受体封闭抗体、抑制剂以及RNA干扰技术等对相应机制进行验证。本研究可阐明IFN-λ调节金葡菌感染的作用及其机制，为进一步研究IFN-λ抑制鼻黏膜病毒和金葡菌共感染奠定理论基础，为临床提供除抗生素以外控制鼻部细菌感染的可能性，开启临床治疗CRSwNP新思路。

Viruses and bacteria play a vital role in pathogenesis of CRSwNP. Eradication of viruses and bacteria in upper airway is a prospective way to alleviate the inflammation in CRSwNP. IFN-λ has anti-viral activity in airway mucosa. Here, we will investigate whether IFN-λ has anti-bacterial ability, hoping to find a new way to control both viral and bacterial infections and provide a new strategy for CRSwNP treatment. We have successfully established staphylococcus aureus ex vivo model. Furthermore, we will evaluate the role of IFN-λ on staphylococcus aureus in nasal tissue during infection by counting the colony number of bacteria. To explore underlying mechanisms, the influence of IFN-λ on macrophages and epithelial barrier molecules such as tight junctions, mucins and anti-bacterial peptides upon IFN-λ stimulations will be observed. In the end, receptor blocking antibodies, inhibitors and RNAi will be used to further confirm the mechanisms. This project may declare the underlying mechanisms by which IFN-λ affects bacterial infections. It will provide theoretical evidences for the influence of IFN-λ on viral and bacterial co-infections. Beside of using antibiotics, we expect to develop new antibacterial strategies, which will broaden the treatments of CRSwNP.