Abstract
Background Clinically severe infection-related inflammation after major liver resection may cause hyperbilirubinemia. This study aims to clarify the impact of bacterial infection and endotoxins on the hepatobiliary transporter system and to explore possible mechanisms of endotoxin-related postoperative hyperbilirubinemia. Method Mice that underwent major hepatectomy with removal of at least 70% of liver volume were exposed to lipopolysaccharide (LPS) at different dosages. Subsequently, hepatobiliary transporter compounds related to bile salt excretion were further investigated. Results The expression of genes related to hepatobiliary transporter compounds was not significantly different in the liver tissue of mice after major hepatectomy and LPS exposure. However, bile salt export pump (BSEP) protein expression within the liver tissue of mice treated with LPS after major hepatectomy was relatively weaker and was even further reduced in the high-dose LPS group. The formation of antibodies against the BSEP in response to endotoxin exposure was also detected. Conclusion This study illustrates a possible mechanism whereby the dysfunction of hepatobiliary transporter systems caused by endotoxin-induced autoantibodies may be involved in the development of postoperative jaundice associated with bacterial infection after major hepatectomy.
Highlights
Liver resection for the removal of tumours is considered best practice for treating hepatic malignancy and can nowadays be performed safely with low mortality and morbidity [1, 2]
The reasons for the development of postoperative jaundice remain unknown; jaundice is known to be caused by defects in the hepatobiliary transporter systems that are important for normal bile salt excretion, leading to cholestasis [9,10,11]
The reasons for the development of postoperative jaundice remain unknown, but it is known that jaundice can be caused by defects in hepatobiliary transporter systems that are important for normal bile salt excretion
Summary
Liver resection for the removal of tumours is considered best practice for treating hepatic malignancy and can nowadays be performed safely with low mortality and morbidity [1, 2]. Severe infection-related inflammation may result in hyperbilirubinemia after liver resection, which might be associated with higher rates of morbidity and mortality [7, 8]. The present study aims to clarify the impact of bacterial infection and endotoxins on the hepatobiliary transporter system and to explore the possible mechanism of endotoxin-related postoperative cholestasis. This study aims to clarify the impact of bacterial infection and endotoxins on the hepatobiliary transporter system and to explore possible mechanisms of endotoxin-related postoperative hyperbilirubinemia. The expression of genes related to hepatobiliary transporter compounds was not significantly different in the liver tissue of mice after major hepatectomy and LPS exposure. This study illustrates a possible mechanism whereby the dysfunction of hepatobiliary transporter systems caused by endotoxin-induced autoantibodies may be involved in the development of postoperative jaundice associated with bacterial infection after major hepatectomy
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