Abstract
Background: Cirrhosis is a common chronic liver disease characterized by irreversible diffuse liver damage. Intestinal microbiome dysbiosis and metabolite dysfunction contribute to the development of cirrhosis. Lactitol (4-β-D-galactopyranosyl-D-glucitol) was previously reported to promote the growth of intestinal Bifidobacteria. However, the effect of lactitol on the intestinal microbiome and fecal short-chain fatty acids (SCFAs) and bile acids (BAs) and the interactions among these factors in cirrhotic patients pre- and post-lactitol treatment remain poorly understood.Methods: Here, using shotgun metagenomics and targeted metabolomics methods.Results: we found that health-promoting lactic acid bacteria, including Bifidobacterium longum, B.pseudocatenulatum, and Lactobacillus salivarius, were increased after lactitol intervention, and significant decrease of pathogen Klebsiella pneumonia and associated antibiotic resistant genes /virulence factors. Functionally, pathways including Pseudomonas aeruginosa biofilm formation, endotoxin biosynthesis, and horizontal transfer of pathogenic genes were decreased in cirrhotic patients after 4-week lactitol intervention compared with before treatment.Conclusion: We identified lactitol-associated metagenomic changes, and provide insight into the understanding of the roles of lactitol in modulating gut microbiome in cirrhotic patients.
Highlights
Cirrhosis is a common chronic liver disease characterized by irreversible diffuse liver damage
We examined the correlation between the microbiome and metabolites and found shifts of the abundance of microbial antibiotic-resistant genes (ARGs), virulence factor genes (VFGs) in microbiome, and metabolites including short-chain fatty acids (SCFAs) and bile acids (BAs)
We found that alterations in the composition of lactitol-treated VFGs were correlated with the strain-level changes in K.pneumonia, which accounted for shifts in the highest proportion of differentiated VFGs in the gut microbiome of patients in lactitol group (LC)-pre vs. LC-post groups
Summary
Cirrhosis is a common chronic liver disease characterized by irreversible diffuse liver damage It is an important risk factor for hepatocellular carcinoma and hepatic decompensation development. Antiviral drug treatments fail to effectively prevent the progression to liver cirrhosis or its associated complications, which suggests that hepatitis virus replication is not the only driving force of cirrhosis development in China [1, 2]. The effect of lactitol on the intestinal microbiome and fecal short-chain fatty acids (SCFAs) and bile acids (BAs) and the interactions among these factors in cirrhotic patients pre- and post-lactitol treatment remain poorly understood
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