Branched-chain amino acids protect the liver from cirrhotic injury via suppression of activation of lipopolysaccharide-binding protein, toll-like receptor 4, and signal transducer and activator of transcription 3, as well as Enterococcus faecalis translocation

Iwasa, Motoh; Tamai, Youichi; Tempaku, Mina; Takamatsu, Shinji; Miyoshi, Eiji; Hasegawa, Hiroshi; Kobayashi, Yoshinao; Takei, Yoshiyuki

doi:10.1016/j.nut.2021.111194

Cited by 20 publications

(15 citation statements)

References 41 publications

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“…E. faecalis translocation to the liver leads to detrimental inflammation for the host in several rodent models by extracellular bacteria. 14 , 16 , 48 The intracellular location of E. faecalis in hepatocytes may be a protective niche against immune detection and may favor the establishment of E. faecalis in the liver. If extracellular E. faecalis has been shown to mediate inflammation in the liver upon intestinal translocation in a mouse model, 14 , 16 , 48 the possibility of intracellular E. faecalis within hepatocytes contributing to liver disorders has not been considered thus far.…”

Section: Discussionmentioning

confidence: 99%

The unforeseen intracellular lifestyle of Enterococcus faecalis in hepatocytes

et al. 2022

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Enterococcus faecalis is a bacterial species present at a subdominant level in the human gut microbiota. This commensal turns into an opportunistic pathogen under specific conditions involving dysbiosis and host immune deficiency. E. faecalis is one of the rare pathobionts identified to date as contributing to liver damage in alcoholic liver disease. We have previously observed that E. faecalis is internalized in hepatocytes. Here, the survival and fate of E. faecalis was examined in hepatocytes, the main epithelial cell type in the liver. Although referred to as an extracellular pathogen, we demonstrate that E. faecalis is able to survive and divide in hepatocytes, and form intracellular clusters in two distinct hepatocyte cell lines, in primary mouse hepatocytes, as well as in vivo . This novel process extends to kidney cells. Unraveling the intracellular lifestyle of E. faecalis , our findings contribute to the understanding of pathobiont-driven diseases.

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Section: Discussionmentioning

confidence: 99%

The unforeseen intracellular lifestyle of Enterococcus faecalis in hepatocytes

et al. 2022

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Section: Discussionmentioning

confidence: 99%

“…Identifying factors that contribute to the onset and progression of liver injury is necessary to improve the management of patients with liver diseases. E. faecalis translocation to the liver leads to detrimental inflammation for the host in several rodent models by extracellular bacteria 14, 16, 48 . The intracellular location of E. faecalis in hepatocytes may be a protective niche against immune detection and may favor the establishment of E. faecalis in the liver.…”

Section: Discussionmentioning

confidence: 99%

“…The intracellular location of E. faecalis in hepatocytes may be a protective niche against immune detection and may favor the establishment of E. faecalis in the liver. If extracellular E. faecalis has been shown to mediate inflammation in the liver upon intestinal translocation in a mouse model 14, 16, 48 , the possibility of intracellular E. faecalis within hepatocytes contributing to liver disorders has not been considered thus far. Further studies will help to determine how this novel intracellular lifestyle may contribute to liver diseases and possibly other diseases.…”

Section: Discussionmentioning

confidence: 99%

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The unforeseen intracellular lifestyle of Enterococcus faecalis in hepatocytes

Nunez

Derré-Bobillot

Lakisic

et al. 2021

Preprint

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Enterococcus faecalis is a bacterial species present at a sub-dominant level in the human gut microbiota. This commensal turns into an opportunistic pathogen under specific conditions involving dysbiosis and host immune deficiency. E. faecalis is also the only intestinal pathobiont identified to date as contributing to liver damage in alcoholic liver disease. We have previously observed that E. faecalis is internalized in hepatocytes. Here, the survival and fate of E. faecalis was examined in hepatocytes, the main epithelial cell type in the liver. Although referred to as an extracellular pathogen, we demonstrate that E. faecalis is able to survive and divide in hepatocytes, and form intracellular clusters in two distinct hepatocyte cell lines, in primary mouse hepatocytes, as well as in vivo. This novel process extends to kidney cells. Unravelling the intracellular lifestyle of E. faecalis, our findings contribute to the understanding of pathobiont-driven diseases.

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“…64 Research on BCAAs oral supplementation has shown decreased fat accumulation in the liver and attenuation of lipotoxic hepatocellular damage in the cirrhotic liver. [65][66][67][68][69] However, several reports revealed that the elevated circulating BCAA was associated with MAFLD and liver injury. 70,71 BCAAs (including valine, leucine, & isoleucine) were found to increase during MAFLD progression as a response to the increased inflammation and oxidative stress.…”

Section: Branched-chain and Aromatic Amino Acids And Metabolic-associated Fatty Liver Diseasementioning

confidence: 99%

The microbial metabolome in metabolic‐associated fatty liver disease

Rajani

Zheng

et al. 2021

J of Gastro and Hepatol

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Metabolism-associated fatty liver disease (MAFLD) is defined as the presence of excess fat in the liver in the absence of excess alcohol consumption and metabolic dysfunction. It has also been described as the hepatic manifestation of metabolic syndrome. The incidence of MAFLD has been reported to be 43-60% in diabetics, ~90% in patients with hyperlipidemia, and 91% in morbidly obese patients. Risk factors that have been associated with the development of MAFLD include male gender, increasing age, obesity, insulin resistance, diabetes, and hyperlipidemia. All of these risk factors have been linked to alterations of the gut microbiota, that is, gut dysbiosis. MAFLD can progress to non-alcoholic steatohepatitis with the presence of inflammation and ballooning, which can deteriorate into cirrhosis, MAFLD-related hepatocellular carcinoma, and liver failure. In this review, we will be focused on the role of the gut microbial metabolome in the development, progression, and potential treatment of MAFLD.

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Branched-chain amino acids protect the liver from cirrhotic injury via suppression of activation of lipopolysaccharide-binding protein, toll-like receptor 4, and signal transducer and activator of transcription 3, as well as Enterococcus faecalis translocation

Cited by 20 publications

References 41 publications

The unforeseen intracellular lifestyle of Enterococcus faecalis in hepatocytes

The unforeseen intracellular lifestyle of Enterococcus faecalis in hepatocytes

The unforeseen intracellular lifestyle of Enterococcus faecalis in hepatocytes

The microbial metabolome in metabolic‐associated fatty liver disease

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