Streptococcus oralis (S. oralis) has been recognized as a fatal pathogen to cause multiorgan failure by contributing to the formation of microthrombus. Coagulation and fibrinolysis systems have been found under the control of circadian clock genes. This study aimed to explore the correlation between BMAL1 and coagulation factor biosynthesis in S. oralis infection. Mice were administered S. oralis to induce sepsis, and HepG2 cells were also infected by S. oralis. The expression of BMAL1 of hepatocytes was downregulated in the S. oralis infection group, leading to the downregulation of coagulation factor VII (FVII) and the upregulation of the coagulation factor XII (FXII) in vitro and in vivo. Furthermore, we confirmed that the deficiency of BAML1 contributed to the elevation of FVII and the decline in FXII by constructing BMAL1-deficiency (Bmal1^−/−) mice. The current result showed that BMAL1 regulates FVII directly. Thus, a novel insight into the coagulation abnormality in S. oralis infection was gained that may optimize the treatment of sepsis by rescuing the expression of BMAL1 in the liver.

口腔链球菌（S. oralis) 已被认为是一种致命的病原体，通过促进微血栓的形成而导致多器官衰竭。已经发现凝血和纤维蛋白溶解系统在生物钟基因的控制下。本研究旨在探讨两者之间的相关性BMAL1和凝血因子的生物合成口腔链球菌感染。给予小鼠口腔链球菌诱导脓毒症，HepG2 细胞也被口腔链球菌. 的表达BMAL1肝细胞在口腔链球菌感染组，导致凝血因子 VII (FVII) 的下调和凝血因子 XII (FXII) 的上调体外和体内. 此外，我们确认了BAML1通过构建 BMAL1 缺陷导致 FVII 升高和 FXII 下降（BMAL1^-/- ) 老鼠。目前的结果表明BMAL1直接调节FVII。因此，对凝血异常的新见解口腔链球菌获得的感染可能通过挽救肝脏中 BMAL1 的表达来优化脓毒症的治疗。