补体C3在S.aureus诱导鼠巨噬细胞分泌IL-1β中的作用及其机制研究

金黄色葡萄球菌（S.aureus）为革兰阳性菌（G+），是一种人畜共患病的重要致病菌。在S.aureus激活补体过程中，我们发现沉积菌体表面的C3成分，除了具有增强吞噬功能外，还可以影响IL-1β的分泌，具体表现为C3-S.aureus在感染鼠巨噬细胞时，与S.aureus感染组相比，胞内pro-IL-1β和IL-1β的表达量明显增高；被巨噬细胞吞噬后，C3-S. aureus感染组胞内成熟的IL-1β的表达量明显减少，其机制并不清楚。我们拟从以下两方面进行探索： C3-S.aureus可以同时激活TLR2和CR3受体，两者间发生crosstalk影响pro-IL-1β的形成；随着S.aureus进入到胞内的C3，与其互作蛋白结合，调节IL-1β的成熟。希望通过上述研究，可以揭示补体C3在S.aureus诱导巨噬细胞分泌IL-1β过程中的作用及其机制。

Staphylococcus aureus (S.aureus) is a Gram-positive bacteria (G +), which is an important pathogen of zoonosis. During the activation of complement by S. aureus, we found that the C3 component deposited on the bacterial surface, not only enhanced phagocytosis of macrophages, but also affected the secretion of IL-1 β. Compared with the S. aureus infected group, the expression of pro-IL-1β and IL-1β in the cell was increased significantly in C3-S.aureus infected group. Furthermore, when C3-S.aureus was swallowed by macrophages, the expression of mature IL-1 β was significantly reduced, compared with the S. aureus group, and its mechanism was not clear. We intend to explore from the following two aspects: C3-S. aureus can simultaneously activate TLR2 and CR3 receptors on macrophages, and crosstalk between them affects the formation of pro-IL-1β; the complement C3 deposited on the bacterial surface, binds with its interacting protein, and regulates the maturation of IL-1β by influencing the formation of inflammatory bodies. It is hoped that the above study can reveal the mechanism of complement C3 mediated secretion of IL-1β during S.aureus phagocytosis by mouse phagocytes.