Good cholesterol protects the liver from inflammation. Free Technical Library News

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Good cholesterol protects the liver from inflammation

30.07.2021

"Good" and "bad" cholesterol are called different types of lipoprotein particles - large transport complexes of lipids and proteins. "Bad cholesterol", that is, low-density lipoproteins (LDL, or LDL), are bad because they increase the likelihood of atherosclerosis: lipids from such particles tend to accumulate in the walls of blood vessels, contributing to the formation of atherosclerotic plaques. "Good cholesterol", that is, high-density lipoproteins (HDL, or HDL), are good in that they do not increase the likelihood of atherosclerosis. At the same time, it is believed that it is best when both "bad" and "good" cholesterol float in the blood less.

However, both low and high density lipoproteins have varieties. And among the "good cholesterol" there are particles called HDL3, which are good for the liver. The fact is that from time to time bacterial lipopolyscharide, fragments of the cell wall of bacteria living in the intestine, enters the liver. These bacterial fragments cause immune cells to react, and a flaccid inflammation begins in the liver. And as you know, inflammation harms not only infections, but also healthy tissues; due to inflammation, healthy cells die, they are replaced by connective tissue, and as a result, the organ no longer functions as well as it should.

Employees of Washington University in St. Louis write in Science that "good" lipoprotein particles such as HDL3 enter the liver along with the blood and interact here with the LBP protein, or lipopolysaccharide-binding protein. As the name suggests, LBP traps bacterial lipopolysaccharide and in doing so stimulates immune cells in the liver. But if LBP has connected with HDL3, then it does not react to bacterial fragments and does not stimulate immune cells.

In mice that did not produce enough HDL3 (due to genetic manipulation or because the part of the intestine in which HDL3 is formed was removed from them), inflammation in the liver increased so much that it led to fibrosis, connective tissue degeneration. Debris of bacterial cells, of course, should be removed in a timely manner, but the immune signals in the liver that arise in response to bacterial debris are unreasonably strong, and local immune cells start completely unnecessary inflammation here. If HDL3 is present in sufficient quantity, they curb inflammation. What's more, there are now experimental drugs that increase HDL3 levels, and these drugs have been able to reduce liver inflammation in mice and keep the liver healthy.

Molecular complexes of HDL3 and LBP are also formed in humans, which means that the same mechanism of protection of the liver can work in us. If this is the case, then it remains only to develop HDL3-enhancing drugs for humans - such drugs could be a good remedy for various liver diseases associated with inflammatory processes.

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