Abstract
The recognition that some eicosanoids are potent inflammatory mediators was based on initial findings of the smooth muscle, microvascular, epithelial cell and nociceptive neural effects of prostaglandins (PGs) and peptidoleukotrienes, which mimicked the major humoral manifestations of tissue inflammation (1–3). The leukocytic component of inflammation also was shown to be reproduced by leukotriene B4 (LTB4) and several di-hydroxy-eicosatetraenoic acids (di-HETEs) from the 15-lipoxygenase (15-LO) pathway, with only modulatory influences of cyclooxygenase products, peptidoleukotrienes and lipoxins (4,5). The eicosanoids often are generated first at sites of inflammation by resident cells responding to the inciting stimulus. For example, neutrophils accumulate in the lungs of individuals lacking alpha 1-antitrypsin as a result of the chemotactic activity of LTB4 produced by alveolar macrophages activated through binding of uninhibited elastase (6). Neutrophil recruitment to the sites of immune complex deposition (7) and substance P release from sensory nerves (8) similarly are responses in part to LTB4 that is produced by activated resident mast cells, as evidenced by the lesser neutrophil responses in mast cell-deficient mice. In inflammatory reactions, the effects of individual eicosanoid mediators may be manifested separately (9), but most often there are substantial interactions both among the eicosanoids and between eicosanoids and mediators from other systems (10–12).
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Zeng, L., An, S., Goetzl, E.J. (1996). EP Receptor Subtype-Dependence of Regulation of Immune Cellular Functions by Prostaglandin E2. In: Vanderhoek, J.Y. (eds) Frontiers in Bioactive Lipids. GWUMC Department of Biochemistry and Molecular Biology Annual Spring Symposia. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5875-0_23
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