Abstract
Chronic consumption of excess ethanol increases the risk of colorectal cancer. The pathogenesis of ethanol-related colorectal cancer (ER-CRC) is thought to be partly mediated by gut microbes. Specifically, bacteria in the colon and rectum convert ethanol to acetaldehyde (AcH), which is carcinogenic. However, the effects of chronic ethanol consumption on the human gut microbiome are poorly understood, and the role of gut microbes in the proposed AcH-mediated pathogenesis of ER-CRC remains to be elaborated. Here we analyse and compare the gut microbiota structures of non-alcoholics and alcoholics. The gut microbiotas of alcoholics were diminished in dominant obligate anaerobes (e.g., Bacteroides and Ruminococcus) and enriched in Streptococcus and other minor species. This alteration might be exacerbated by habitual smoking. These observations could at least partly be explained by the susceptibility of obligate anaerobes to reactive oxygen species, which are increased by chronic exposure of the gut mucosa to ethanol. The AcH productivity from ethanol was much lower in the faeces of alcoholic patients than in faeces of non-alcoholic subjects. The faecal phenotype of the alcoholics could be rationalised based on their gut microbiota structures and the ability of gut bacteria to accumulate AcH from ethanol.
Highlights
In living systems, ethanol induces the formation of reactive oxygen species (ROS), which promote oxidative stress via a variety of cellular processes[5,6]
The relative abundance of Bacteroidetes was significantly decreased in the gut microbiota (GM) of the alcoholic patients while Proteobacteria were apparently enriched, though the enrichment was statistically insignificant (Supplementary Fig. S2)
Using a mouse model, Bull-Otterson et al.[22] reported that chronic ethanol consumption lowers the abundances of Bacteroidetes and Firmicutes and enhances Proteobacteria and Actinobacteria. These results suggest that chronic ethanol consumption generally diminishes the Bacteroidetes and enriches the Proteobacteria in the GM, regardless of human race and even animal species
Summary
Ethanol induces the formation of reactive oxygen species (ROS), which promote oxidative stress via a variety of cellular processes[5,6]. How the chronic consumption of large amounts of ethanol affects human GM structures and the bacteriocolonic pathway of ethanol oxidation (see above) is not known, the GM structures and ethanol metabolism of intestinal bacteria might be related to ER-CRC pathogenesis To better understand these issues, a basic investigation using bacterial ecology and physiology approaches is needed. The GM of alcoholics showed more phylogenetic diversity (β-diversity) than those of non-alcoholics, with a diminution of dominant obligate anaerobes such as Bacteroides, Bifidobacterium, and Ruminococcus and an enrichment of Streptococcus and many other minor bacterial species This finding might be at least partially explained by the intestinal oxidative stress induced by chronic ethanol exposure, to which obligate anaerobes are susceptible. These observations provide important information for understanding the mechanisms of ER-CRC pathogenesis
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