Antibody Blocks Inflammation in Mice Model for Arterial Hardening

Published By : 07 Jun 2018 | Published By : QYRESEARCH

According to a recent research study undertaken by researchers from the University of California (UC) San Diego School of Medicine, a naturally occurring antibody that attaches OxPL (oxidized phospholipids) molecules on the surfaces of cells that are modified due to inflammation can block further inflammation in mice. It was found in the study that even when the mice subjects were given a high-fat diet, the antibody arrested the formation of plaque formation in arteries, thus protecting them from liver disease, arterial hardening, and helped prolonged their lives.

The study is the first time it has been demonstrated that in living organisms, OxPL can lead to the formation of arterial plaque and trigger inflammation. The results of the study suggest a new way of reversing or prevention several inflammatory diseases.

Wherever the body suffers from inflammation, it gets OxPL. This does not necessarily mean that the molecule is the cause for inflammation but it certainly plays a key role in causing the inflammation. Some phospholipids-the class of lipids that are a major constituent element of cell membranes-are susceptible to modifications when they come in contact with reactive species of oxygen, leading to the formation of OxPL. This is highly common in inflammations-related conditions such as atherosclerosis. Before the study, researchers could not control the oxidation of phospholipid in a way that would enable them the proper study of OxPL’s role in atherosclerosis or inflammation.

The study suggests that the treatment methods that are capable of inactivating OxPL may prove to be beneficial for the reduction of inflammation in generation, particularly when it comes to controlling inflammation in conditions such as aortic stenosis, hepatic steatosis, and atherosclerosis. The research team is now testing the antibody in mouse models of human conditions associated with inflammation, such as nonalcoholic steatohepatitis and osteoporosis.

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