Bacillus amyloliquefaciens SC06 Attenuated Lipopolysaccharide-Induced acute liver injury by suppressing bile acid-associated NLRP3 inflammasome activation.

• B. amyloliquefaciens SC06 exhibited protective properties against hepatic inflammation and hepatocyte necrosis induced by LPS through inhbit the bile acid-associated-NLRP3 inflammasome pathway. • B. amyloliquefaciens SC06 administration efficiently overcomes LPS-induced bile acid metabolism anomalies. • B. amyloliquefaciens SC06 was unable to directly inhibit the activation of NLRP3 inflammasome. • Taurochenodeoxycholic acid (TCDCA) activated inflammatory vesicles and exacerbates LPS-induced inflammatory injury. The involvement of the inflammatory response has been linked to the development of liver illnesses. As medications with the potential to prevent and cure liver illness, probiotics have garnered an increasing amount of interest in recent years. The present study used a piglet model with acute liver injury (ALI) induced by lipopolysaccharides (LPS) to investigate the regulatory mechanisms of Bacillus amyloliquefaciens SC06. Our findings indicated that SC06 mitigated the liver structural damage caused by LPS, as shown by the decreased infiltration of inflammatory cells and the enhanced structural integrity. In addition, After the administration of SC06, there was a reduction in the increased levels of the liver damage markers. In the LPS group, there was an increase in the mRNA expression of inflammatory cytokines, apoptosis cell rate, and genes associated with apoptosis, while these alterations were mitigated by SC06 administration. Furthermore, SC06 prevented pigs from suffering liver damage by preventing the activation of the NLRP3 inflammasome, which was normally triggered by LPS. The examination of serum metabolic pathways found that ALI was related to several metabolic processes, including primary bile acid biosynthesis, pentose and glucuronate interconversions and the metabolism of phenylalanine. Significantly, our research revealed that the administration of SC06 effectively controlled the concentrations of bile acids in the serum. The correlation results also revealed clear relationships between bile acids and liver characteristics and NLRP3 inflammasome-related genes. However, in vitro experiments revealed that SC06 could not directly inhibit NLRP3 activation under ATP, monosodium urate, and nigericin stimulation, while taurochenodeoxycholic acid (TCDCA) activated NLRP3 inflammasome related genes. In conclusion, our study proved that the hepaprotective effect of SC06 on liver injury, which was closely associated with the restoration of bile acids homeostasis and NLRP3 inflammasome inhibition. [ABSTRACT FROM AUTHOR]