在炎症性疾病发生发展过程中，凝血酶是启动凝血与炎症的关键因子之一。凝血酶原的激活依赖凝血酶原酶Fgl2的催化。Fgl2包括跨膜型(mFgl2)和可溶型(sFgl2)两类：mFgl2能直接催化凝血酶原转变为凝血酶，快速启动凝血；sFgl2则发挥免疫抑制作用。炎症消退是主动的程序化过程，已知Fgl2可促进多种炎症启动，但其对炎症消退的影响尚不清楚。我们前期预实验发现Fgl2在临床败血症患者血浆中表达上调，Fgl2敲除小鼠的腹膜炎较野生小鼠更严重，sFgl2可促进巨噬细胞表达促消退脂类介质合成的关键酶15-LOX，从而推测mFgl2和sFgl2在炎症消退中可能发挥不同的作用，mFgl2通过促凝血而促炎，而sFgl2可诱导SPM的合成而促进炎症消退。本课题拟阐明Fgl2对炎症的程序化启动和和消退过程的调控及具体机制，为启动炎症消退提供新的靶点，为临床抗败血症治疗提供新思路。

In the development of inflammatory diseases, thrombin is a key factor in the activation of blood clotting and inflammation. Prothrombin activation is dependent on the catalysation of prothrombinase Fgl2. Fgl2 includes 2 distinct forms, i.e. transmembrane (mFgl2) and soluble (sFgl2): mFgl2 directly cleaves prothrombin into thrombin, which subsequently activates clotting; sFgl2 plays an immunosuppressor role. Inflammation resolution is an active programmed process. It has been reported that Fgl2 can promote the onset of a variety types of inflammation, but its impact on inflammation resolution is unclear. Our preliminary experiments found that Fgl2 was upregulated in the plasma of patients with clinical sepsis; the peritonitis in Fgl2 knockout mice is more severe than in wild-type mice, sFgl2 can promote 15-LOX, a key enzyme in the synthesis of specialized pro-resolving lipid mediators, in macrophages. Hence we propose the hypothesis that mFgl2 and sFgl2 may play a different role in the inflammation resolution, mFgl2 is pro-inflammatory via its procoagulant role, while sFgl2 can induce the synthesis of the SPM and promote inflammation resolution. This paper intends to elucidate the role and regulatory mechanism of Fgl2 in the programmed onset and resolution of inflammation, thereby provide novel targets for eliciting resolution and new ideas for clinical anti-sepsis treatment.