Inflammation and Atherosclerosis

Abstract

An initial chemical, mechanical or immunological insult induces endothelial dysfunction. This triggers a cascade of inflammatory reactions, in which monocytes, macrophages, T lymphocytes and vascular smooth muscle cells participate. Leukocyte adhesion molecules, cytokines, growth factors and metalloproteinases participate in all stages of atherogenesis. Almost all of the traditional risk factors for atherosclerosis are associated with and participate in the inflammatory process. Many infectious agents, mainly Chlamydia pneumoniae, have been proposed as potential triggers of the cascade. The immune system has been implicated in plaque formation, through the activation of cellular and humoral immunity against innate or microbial heat shock protein 60. Methods of detection of systemic or local plaque inflammation have been developed and research is being conducted on the potential use of anti-inflammatory and antibiotic drugs in atherosclerosis.

S‐Allyl‐L‐Cysteine Sulfoxide Inhibits Tumor Necrosis Factor‐Alpha Induced Monocyte Adhesion and Intercellular Cell Adhesion Molecule‐1 Expression in Human Umbilical Vein Endothelial Cells

“…Endothelial dysfunction in the arterial wall is associated with inflammation, which has been thought to trigger leukocyte adhesion, platelet aggregation, and vascular smooth muscle cell proliferation and migration, leading to thickening of the arterial wall and the formation of atherosclerotic lesion (Kaperonis et al, 2006). During the process of atherosclerosis, immune cells such as monocytes, macrophages, T and B cells can adhere onto endothelial cells and elicit acute coronary syndromes (Hansson, 2005).…”

Pro-inflammatory effect of fibrinogen on vascular smooth muscle cells by regulating the expression of PPARα, PPARγ and MMP-9

“…Clinical and experimental studies show the consistent association between various markers of inflammation and cardiovascular diseases (2,3). Previous studies indicated the important roles of pro-inflammatory cytokines in the pathogenesis of atherosclerosis, such as C-reactive protein (CRP) (4,5), interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α) (6,7).…”

Triple immunofluorescence labeling of atherosclerotic plaque components in apoE/LDLR -/- mice.

“…Another component of the plaque, smooth muscle cells from the vascular media, proliferate and migrate into the lesion area [3]. It is now clear that activation of macrophages, T lymphocytes as well as smooth muscle cells determines the outcome of the atherosclerosis [4]. Hence, good methods of assessment of the distribution and abundance of these three cell types in the plaque are mandatory for better understanding of multicellular mechanisms involved in the plaque formation and for estimation of the anti-atherosclerotic treatment effects.…”