On the potential role of intestinal microbial community in hepatocarcinogenesis in chronic hepatitis B

Abstract

The chronic infection of hepatitis B virus (HBV) is the most potent risk factor for the development of cirrhosis and hepatocellular carcinoma (HCC). The association of intestinal microbiota alteration with progressive liver disease has been investigated in recent studies. Overgrowth of potentially pathogenic bacteria of gram‐negative species and, in particular, a significant increase in the fecal count of Escherichia coli (E. coli) are characterized in the presence of HCC. This study was conducted to describe the characteristics of the intestinal microbiota related to the presence of HCC in HBV‐carrier patients. The available literature indicates the colonization of E. coli as principal source of portal vein lipopolysaccharide (LPS), in the gut may contribute to the carcinogenesis process by inducing chronic inflammation. This understanding could help to predict the clinical outcomes in HBV‐carrier patients and innovative strategies to reduce the virulence of liver disease from intestinal dysbiosis.

Demystifying the manipulation of host immunity, metabolism, and extraintestinal tumors by the gut microbiome

“…384 Both mice and patients with HCC characteristically display failing intestinal barrier integrity and gut dysbiosis, as well as high levels of circulating LPS, which serves as an inducer of inflammation to expedite liver fibrosis. 384,385 In mice with dimethylnitrosamine-induced hepatocarcinogenesis, due to the failing intestinal barrier, LPS can enter the liver and bind to TLR4 on hepatocytes, hepatic stellate cells (HSCs) and Kupffer cells, which facilitates tumor progression through multiple mechanisms. 386,387 In HSCs, the LPS/TLR4 pathway triggers upregulation of the hepatomitogen epiregulin, which belongs to the epidermal growth factor family and has a potent mitogenic effect on hepatocytes, thereby inhibiting hepatocyte apoptosis.…”

Role of Microbiota in Pathogenesis and Management of Viral Hepatitis

“…Lactobacillus, Bifidobacterium, Saccharomyces boulardii, and Lactobacillus plantarum play a bigger role in the management of various metabolic disorders and hepatitis (Mohamadkhani, 2018).…”

“…Despite its crucial role in the synthesis of vitamin K, folate, SCFA, and peroxides, gut microbiota acts as a chief environmental as well as etiological factor for the progression of many liver diseases (O'Hara and Shanahan, 2007 ). Particularly, gut microbiota has a larger influence on alcoholic liver disease, non-alcoholic fatty liver disease, viral hepatitis (hepatitis B and C), autoimmune hepatitis (AIH), primary sclerosing cholangitis (PSC), and primary biliary cholangitis (PBC) (Mohamadkhani, 2018 ). Lactobacillus, Bifidobacterium, Saccharomyces boulardii , and Lactobacillus plantarum play a bigger role in the management of various metabolic disorders and hepatitis (Mohamadkhani, 2018 ).…”

“…Particularly, gut microbiota has a larger influence on alcoholic liver disease, non-alcoholic fatty liver disease, viral hepatitis (hepatitis B and C), autoimmune hepatitis (AIH), primary sclerosing cholangitis (PSC), and primary biliary cholangitis (PBC) (Mohamadkhani, 2018 ). Lactobacillus, Bifidobacterium, Saccharomyces boulardii , and Lactobacillus plantarum play a bigger role in the management of various metabolic disorders and hepatitis (Mohamadkhani, 2018 ).…”

“…In viral hepatitis, few harmful bacteria like Escherichia coli, Enterobacteriaceae, Enterococcus faecalis, and Faecalibacterium prausnitzii directly alter the profile of good intestinal microbiota with a lower number of intestinal lactic acid species such as Lactobacillus, Pediococcus, Weissella , and Leuconostoc (Bajaj et al, 2014 ; Chen et al, 2016 ). Some of the bacterial species, i.e., Neisseria, E. coli, Enterobacteriaceae, E. faecalis, F. prausnitzii , and Gemella , are also found responsible for the progression of hepatitis B and C virus–related cirrhosis and primary biliary cirrhosis (Chen et al, 2016 ; Mohamadkhani, 2018 ). Candida is also frequently found in patients with hepatitis B–related cirrhosis (Cui et al, 2013 ).…”