It has been suggested that LPS can prevent arteriosclerosis.
“Arteriosclerosis” in most cases refers to atherosclerosis. “Atheromatous” is a word that refers to a state of “rice porridge,” hence, “atherosclerosis” is the state in which “rice porridge”-like cholesterol plaque occurs in the artery.
When a blood vessel is damaged, cholesterol-carrying LDL gets trapped in the intima, where the LDL is oxidized, builds up as waste, and is normally phagocytosed by macrophages. After phagocytosed, the residual cholesterol is transferred to HDL for recycling. However, when there is too much oxidized LDL for macrophages to process, they die while still containing the oxidized LDL. This leaves a deposit of atheromatous cholesterol, which is also called plaque. As plaque builds up, the blood vessel may narrow or a thrombus may form when the plaque is ruptured.
This explanation could be misinterpreted as macrophage activation promoting arteriosclerosis. But this is not. The risk of arteriosclerosis becomes higher only when there is too much oxidized LDL for the macrophages to process. The blood is kept clean as long as macrophages are active. It is therefore assumed that macrophage-activating LPS is also effective in preventing arteriosclerosis.
A study in which arteriosclerotic model mice were fed with a high-fat diet showed that those that had ingested LPS had suppressed weight gains, and lower levels of aortic plaque deposition compared with those that had not ingested LPS (*1).
(*1) Oral administration of Pantoea agglomerans-derived lipopolysaccharide prevents development of atherosclerosis in high-fat diet-fed apoE-deficient mice via ameliorating hyperlipidemia, pro-inflammatory mediators and oxidative responses, PLOS ONE, https://doi.org/10.1371/journal.pone.0195008 March 27, 2018
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