High levels of low-density lipoprotein (LDL) cholesterol can be very dangerous. These high levels of LDL can cause blockages of plaque in the arteries as well as cause other diseases. High-density lipoprotein (HDL), however, helps deter inflammation and plaque buildup in the arteries.
Researchers recently found that high levels of HDL alone will not stop inflammation caused from plaque in the arteries from occurring. This large team of researchers from the USA and other parts of the world used genomic and bioformatic methods to find out how HDL works. They found a gene in phagocytic cells that acts on the immune system as a defense against foreign bodies in the bloodstream. Toll-like receptors (TLR) help these phagocytes sift through these foreign bodies and focus on the harmful ones. When TLR finds a harmful foreign body, it causes an inflammatory reaction to occur. A transcriptional regulator called ATF3 is also activated. The transcriptional regulator uses TLR to reduce inflammation.
This inflammatory process holds off pathogens and repairs damaged tissue. If the inflammatory process does not make a quick turnaround, organ failure and other serious maladies can occur. The transcriptional regulator suppresses the inflammatory process and brings it under control, however. It is the action of high-density lipoprotein (HDL) that activates the transcriptional regulator (ATF3). Therefore, HDL is responsible for reducing inflammation. However, HDL does not work alone in reducing inflammation levels. In the future, molecular levels may be used to treat inflammation caused by diabetes and other inflammatory diseases.