We hypothesize that endogenous IL-32 in liver cells, a human monocytic cell line and carotid plaque tissue, can affect atherosclerosis by regulating (HDL) cholesterol homeostasis via expression of cholesterol transporters/mediators.
IL-32not only modulates important inflammatory pathways known to contribute to the pathogenesis of both inflammatory diseases and atherosclerosis, including tumor necrosis factor (TNF)α, IL-6 or IL-1β, but it has been also suggested to modulate endothelial cell function and the serum concentration of high-density lipoprotein (HDL).
This study introduces IL-32 as a critical regulator of endothelial function, expanding the properties of this cytokine relevant to coagulation, endothelial inflammation, and atherosclerosis.