ABSTRACT
Figure 4.1 Metabolism of arachidonic acid along the cyclooxygenase and lipoxygenase pathways to generate biologically active mediators, i.e., prostanoids, leukotrienes, and lipoxins. Eicosanoids are hormone-like molecules that exert, in an autocrine and paracrine fashion, complex control over a wide range of physiological processes. Cells of the innate immune system, including tissue macrophages, dendritic cells (DCs), and neutrophils, are the major producers of eicosanoids, which act at nanomolar concentrations, and their effects vary from type to type of cells. Eicosanoid production is considerably increased during inflamm-ation, and their biosynthetic pathways are of particular clinical relevance because their products are involved in the pathogenesis of various pathologies related to immune functions. During inflammation eicosanoids are present and act as proinflammatory molecules via several mechanisms, e.g., chemoattraction (LTB4), platelet aggregation (TxA2), contraction of smooth muscle (cys-LTs, PGs), and modulation of vascular permeability (LTs). On the other hand, LXs appear to play an active role in controlling the resolution of inflammation by stimulating endogenous anti-inflammatory pathways. In the past decades, research has shown that immune cells (mainly macrophages and some T cells) dominate early atherosclerotic lesions, and their effector molecules accelerate progression of the lesions that finally results in the induction of acute coronary syndromes [64]. That is the reason why the scientific community considers atherosclerosis as an inflammatory disease.
