Atherosclerosis is a chronic inflammatory disease that is a major health risk in developed countries. Currently, there are few targeted therapies which can be used to treat or cure the disease. It is clear that atherosclerosis has a very complex pathology, with several genetic and environmental factors. At this point the biochemistry of lesion formation and progression is not well understood. It is known that macrophages play a role in lesion biology, and can modulate the inflammation present in the plaque. The goal of this project is to analyze the role of one macrophage-expressed gene, secretory leukocyte protease inhibitor (SLPI) in the genetic predisposition to atherosclerosis. SLPI is involved in managing inflammation levels during wound healing, and has been shown to interact with innate immune signaling pathways. It was shown that SLPI is more highly expressed in elicited peritoneal macrophages from C57BL/6 mice than FVB/N mice. C57BL/6 mice have both a higher susceptibility to atherosclerosis and a more inflammatory phenotype in general. Whether this difference in SLPI expression has a direct influence on, or is a product of, atherosclerotic disease progression is not known. ? ?
