Washington: A team of researchers has identified a central switch by which High-density lipoprotein (HDL), known colloquially as "good cholesterol", controls the inflammatory response.
Low-density lipoprotein (LDL) is commonly referred to as the "bad cholesterol", because it promotes atherosclerosis. In contrast, the "good cholesterol", high-density lipoprotein (HDL), helps transport excess cholesterol out of the bloodstream and can counteract an inflammatory reaction in damaged vessel walls.
Prof. Eicke Latz, Director of the Institute of Innate Immunity at the University of Bonn said the molecular causes to which this protective effect of HDL can be attributed were unclear until now.
In a very extensive study over a period of about three years, the group performed experiments in human and mouse cells, to determine which genes are regulated by high HDL levels.
"With the aid of genomic and bioinformatics approaches, we were able to filter out a candidate gene from the wealth of regulated genes", Prof. Joachim L. Schultze of the Life and Medical Sciences (LIMES) Institute of the University of Bonn, said.
This gene is found in phagocytes, which act in the body like police on the beat and, as part of the innate immune defense system, arrest intruders. These patrolmen are supported by a kind of "criminal file", the so-called Toll-like receptors (TLR). With their help, the phagocytes can distinguish between "good" and "bad".
If it is a dangerous intruder, the TLR can also trigger the release of inflammatory substances via biochemical signaling pathways. The transcriptional regulator, ATF3, plays a key role in this process.
The study was published in journal Nature Immunology.