炎症作为一种重要的免疫防御手段，在宿主抵御病原微生物感染中发挥着重要作用。申请人前期发现，灿烂弧菌感染刺参过程中同样伴随着炎症反应，并证实刺参IL-17类似物通过调控NF-κB通路影响体腔细胞的迁移和增殖。脊椎动物研究表明IL-17调控炎症功能依赖于与IL-17R的结合。然而刺参IL-17R类似物（IL-17Rh）是否介导炎症反应，以及如何介导炎症反应等关键问题尚不明确，本项目拟通过刺参IL-17Rh抑制表达或过表达探究IL-17Rh参与灿烂弧菌诱导的炎症反应。继而，通过体外结合测定和体内免疫共沉淀明确刺参IL-17介导的炎症依赖于与IL-17Rh的结合。最后，通过检测IL-17Rh异常表达后刺参NF-κB入核水平、以及IκB磷酸化水平变化，初步掌握刺参IL-17Rh调控炎症活化的分子途径。研究成果将为认识海洋无脊椎动物炎症调节机制提供基础，为理解IL-17R的功能进化提供科学依据。

Inflammatory response as an important innate immune mechanism, plays an important role in the host's defense against infection by pathogenic microorganisms. Our previous work has indicated that Vibrio splendidus infection also could induced inflammatory phenomena in Apostichopus japonicus, and it was confirmed that the IL-17 homologue of A. japonicus affected the migration and proliferation of coelomic cells by regulating NF-κB pathway. Vertebrate studies have shown that IL-17 regulation of inflammatory function depends on its binding to IL-17R. However, does A. japonicus IL-17R homologue (IL-17Rh) mediate inflammation? It is not clear how to mediate the inflammatory response and other key issues. In order to further explore the functions of A. japonicus IL-17R and IL-17 homologue in the inflammatory response, this project intends to investigate the IL-17Rh-mediated inflammatory response induced by V. splendidus infection through the inhibition or overexpression of A. japonicus IL-17Rh. Subsequently, through in vitro binding assays and in vivo co-immunoprecipitation, we will demonstrate that the role of IL-17 regulation inflammation in A. japonicus mediated by IL-17Rh. Finally, through detecting the level of NF-κB entering the nucleus, and the changes of IκB protein expression and phosphorylation, we will certify the molecular mechanism of inflammatory activation mediated by IL-17/IL-17R pathway under pathogen infection. The research results will provide reference for understanding and grasping the inflammatory regulation mechanism of marine invertebrates and provide new ideas for the IL-17 functional evolution.