Abstract

Endogenous alcohol produced by the gut microbiome is transported via the bloodstream to the liver for detoxification. Gut dysbiosis can result in chronic excess alcohol production that contributes to the development of hepatic steatosis. The aim of this study was to examine whether linolenic acid can manipulate the production of harmful alcohol and beneficial short-chain fatty acids (SCFAs) in the metabolome of commensal Klebsiella pneumoniae (K. pneumoniae) and the virulent K. pneumoniae K1 serotype. Glucose fermentation by the K. pneumoniae K1 serotype yielded increased production of alcohol and decreased SCFAs (especially acetate and propionate) compared to those of commensal K. pneumoniae. However, the use of linolenic acid instead of glucose significantly reduced alcohol and increased SCFAs in the fermentation media of the K. pneumoniae K1 serotype. The work highlights the value of shaping the microbial metabolome using linolenic acid, which can potentially regulate the gut–liver axis for the prevention and treatment of alcohol-induced liver diseases.

Highlights

  • The human gut microbiome consists of the entirety of the microbes that reside in the human gut [1]

  • The data in this study demonstrate for the first time that linolenic acid, a polyunsaturated ω-3 fatty acid, can lower alcohol production yet induce an increase in short-chain fatty acids (SCFAs) in the fermentation process of the virulent K. pneumoniae K1 serotype

  • Linolenic acid and its derivatives, or linolenic acid-rich foods such as flaxseed, pumpkin, and walnut oils, may function as natural prebiotics to lower the virulence of K. pneumoniae

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Summary

Introduction

The human gut microbiome consists of the entirety of the microbes that reside in the human gut [1]. These microbes aid in human innate immunity, metabolic functions, and overall wellbeing. Certain bacteria residing in the human gut are associated with liver damage via the gut–liver axis. Hypervirulent strains of the capsular serotypes K1 or K2 of K. pneumoniae are known to induce liver abscesses or bacteremia in patients. The literature has demonstrated that the K. pneumoniae K1 serotype in particular can induce primary liver abscesses and is a risk factor for metastasis [4].

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