Bmal1 Regulates Coagulation Factor Biosynthesis In Mouse Liver In Streptococcus Oralis Infection

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 betweenBMAL1and coagulation factor biosynthesis inS. oralisinfection. Mice were administeredS. oralisto induce sepsis, and HepG2 cells were also infected byS. oralis. The expression ofBMAL1of hepatocytes was downregulated in theS. oralisinfection group, leading to the downregulation of coagulation factor VII (FVII) and the upregulation of the coagulation factor XII (FXII)in vitroandin vivo. Furthermore, we confirmed that the deficiency ofBAML1contributed 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 inS. oralisinfection was gained that may optimize the treatment of sepsis by rescuing the expression of BMAL1 in the liver.