And always drunk
Intestinal bacteria caught in alcohol production
Polina Loseva, N+1
Scientists have found out that the cause of non-alcoholic fatty liver disease, which usually occurs due to metabolic problems, can still be ethanol – even if a person does not suffer from alcoholism: in the intestines of a patient with this disease, they found strains of Klebsiella bacteria that produce alcohol. They confirmed their assumptions by transplanting the patient's microbiota to mice: their liver cells also began to accumulate fat, and characteristic symptoms of the disease appeared. The work was published in the journal Cell Metabolism (Yuan et al., Fatty Liver Disease Caused by High-Alcohol-Producing Klebsiella pneumonia).
Fatty liver disease, or steatosis, usually precedes more severe lesions of this organ: cirrhosis, inflammation and the development of carcinoma. Steatosis can occur in humans in two ways. The first is associated with the use of a large amount of alcohol: in the process of ethanol utilization, liver cells produce many by-products that trigger the pathways of fat biosynthesis, and fat droplets form in the cells. The second pathway is associated with systemic metabolic disorders (for example, obesity or diabetes), but its exact mechanisms are still unknown.
Jing Yuan (Jung Yuan) from The Beijing Institute of Pediatrics together with colleagues became interested in the case of a patient with severe liver steatosis. He did not drink alcohol, but consumed a lot of carbohydrates, and the concentration of ethanol in his blood was about 400 mg/ l (this corresponds to 0.4 ppm: in Russia, with such a level of alcohol, for example, it is no longer possible to drive a car). This is a typical manifestation of a rare syndrome of self-intoxication (Eng. auto-brewery syndrome), in which the human body produces ethanol itself. Usually this syndrome is associated with the activity of yeast in the intestine, but antifungal drugs did not change the patient's condition, so scientists concluded that the cause of the disease may be different.
The researchers suggested that the producer of alcohol may be bacteria in the patient's intestines. They isolated bacterial RNA from his stool and sequenced it to determine the species composition of the microbiota. It turned out that representatives of the genus Klebsiella in the patient's intestines is about 900 times more than normal: 18.8 percent instead of the prescribed 0.02. Among them, scientists found two strains of the bacterium Klebsiella pneumoniae, which were not only resistant to alcohol, but also produced it themselves.
To check how common this bacterium is in patients with a similar diagnosis, scientists analyzed the stool of 43 more patients with liver steatosis and 48 healthy people. They found that in comparison with healthy people, the number of bacteria of the genus in the intestines of obese liver patients Klebsiella is slightly increased, but the ability of these bacteria to produce alcohol is much higher. The researchers took repeated stool samples from the same patients six months later: by this time, many of them had recovered from steatosis, and alcohol-producing bacteria in their intestines had become much smaller.
To confirm that it really is a bacterium, scientists conducted experiments on mice: they fed several groups of mice with ordinary food containing alcohol or a high concentration of Klebsiella pneumoniae. It turned out that liver damage occurs in both the second and third groups of animals. Then the scientists took sterile, microbial-free mice and transplanted them with culture Klebsiella: animals also have symptoms of liver steatosis.
Finally, the researchers created model mice in which the condition of a patient with steatosis was completely reproduced: for this purpose, the microbiota of the patient was transplanted to the microbial mice. When transplanting bacteria from these mice to healthy mice, the latter also had all the characteristic symptoms. At the same time, if Klebsiella bacteria were removed before microbiota transplantation, steatosis did not develop in healthy mice.
Thus, scientists have demonstrated that ethyl alcohol can still be to blame for non-alcoholic fatty liver disease: even if a person does not drink at all, his gut microbiota can produce enough alcohol to damage the liver.
Previously, intestinal bacteria have already been accused of aiding the development of a variety of human diseases. Their contribution was found in the occurrence of stroke and Alzheimer's disease.
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