Alcohol allows bacteria to infiltrate into liver

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"Alcohol appears to impair the body’s ability to keep microbes in check. When those barriers breakdown, bacteria that does not normally colonise the liver end up there"

Alcohol allows gut bacteria to migrate to the liver, promoting alcohol—induced liver disease, a new study has warned.

Researchers from University of California (UC), San Diego in U.S. conduced the study in mice and in laboratory samples.

They previously found that chronic alcohol consumption is associated with lower intestinal levels of REG3 lectins, which are naturally occurring antimicrobials.

In the new study, researchers discovered that REG3G deficiency promotes progression of alcohol—induced liver disease.

Mice engineered to lack REG3G and fed alcohol for eight weeks were more susceptible to bacterial migration from the gut to the liver than normal mice who received the same amount of alcohol.

REG3G—deficient mice also developed more severe alcoholic liver disease than normal mice.

To find methods for stemming the tide of liver—damaging microbes, researchers tried experimentally bumping up copies of the REG3G gene in intestinal lining cells grown in the lab.

They found that more REG3G reduced bacterial growth.

Likewise, restoring REG3G in mice protected them from alcohol—induced fatty liver disease, a condition that precedes end—stage cirrhosis.

Liver cirrhosis is also known as end—stage liver disease.

Approximately half of the deaths from this condition are related to alcohol consumption.

Human small intestine samples supported some of the researcher’s finding in mice. Not only do patients with alcohol dependency have lower levels of REG3G than healthy people, they also have more bacteria growing there, the study found.

“Alcohol appears to impair the body’s ability to keep microbes in check. When those barriers breakdown, bacteria that does not normally colonise the liver end up there, and now we have found that this bacterial migration promotes alcohol liver disease,” said Bernd Schnabl from UC.

“Strategies to restore the body’s defences might help us treat the disease,” Mr. Schnabl said.

The findings were published in the journal Cell Host & Microbe.