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Infectious Microecology in Liver Disease

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Part of the book series: Advanced Topics in Science and Technology in China ((ATSTC))

Abstract

More than 100 years ago, Pavlov discovered that the liver can remove enteric toxins. Now we think that, under normal circumstances, the liver can also remove bacteria, fungi, and their metabolites such as toxins, endotoxin, ammonia, indoles, phenols, short-chain fatty acids (C4–C6), pseudo-nerve delivery mass precursors. Gnotobiote research reveals that intestinal flora and endotoxin in the liver increase the number of Kupffer cells and play an important role in the improvement. When the functioning of the liver suffers damage (including chronic hepatitis, alcoholic and non-alcoholic fatty liver disease, cirrhosis, severe hepatitis, liver transplantation, etc.), the system will incur a gut microflora imbalance in varying degrees, damage to the intestinal barrier and allowing intestinal bacteria and its metabolites to enter extra-intestinal organs (including blood) , resulting in abdominal infection, endotoxemia and so on. Meanwhile, the inflammatory stimuli activate the immune system excessively, which can cause an abnormal immune response, leading to systemic inflammatory response syndrome (SIRS) or multiple organ failure, such as gastrointestinal dysfunction or failure. Endotoxemia, and gastrointestinal dysfunction can also increase the imbalance in gut microflora, and further aggravate liver injury, a vicious cycle. Through a series of basic and clinical microbial research of liver diseases, we found that probiotics can adjust the gut microflora, repairing and improving the intestinal barrier function and reducing intestinal bacterial translocation, decreasing endotoxemia, reducing infection and improving the functioning of the liver.

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© 2014 Zhejiang University Press, Hangzhou and Springer-Verlag Berlin Heidelberg

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Li, L. (2014). Infectious Microecology in Liver Disease. In: Li, L. (eds) Infectious Microecology. Advanced Topics in Science and Technology in China. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-43883-1_12

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