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Chapter 19 : Lipid Mediators in Inflammation

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Lipid Mediators in Inflammation, Page 1 of 2

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Abstract:

Before we discuss lipids and their role in homeostasis and host defense, we will recount the essence of the inflammatory response. Inflammation is a reaction of the microcirculation; it’s a protective response initiated after infection or injury. While both local and systemic responses can be activated, inflammation is an essential biological process with the objective of eliminating the inciting stimulus, promoting tissue repair/wound healing, and, in the case of infection, establishing memory such that the host mounts a faster and more specific response upon a future encounter. The acute inflammatory response is a complex yet highly coordinated sequence of events involving a large number of molecular, cellular, and physiological changes. It begins with the production of soluble mediators (complement, chemokines, cytokines, eicosanoids—including prostaglandins [PGs], free radicals, vasoactive amines, etc.) by resident cells in the injured/infected tissue (i.e., tissue macrophages, dendritic cells, lymphocytes, endothelial cells, fibroblasts, and mast cells), concomitant with the upregulation of cell adhesion molecules on both leukocytes and endothelial cells that promote the exudation of proteins and influx of granulocytes from blood ( ). Upon arrival, these leukocytes, typically polymorphonuclear leukocytes (PMNs) in the case of nonspecific inflammation or eosinophils in response to allergens, function primarily to phagocytose and eliminate foreign microorganisms via distinct intracellular (superoxide, myeloperoxidase, proteases, and lactoferrins) and/or extracellular (neutrophil extracellular traps) killing mechanisms ( ). It is likely that the magnitude of the infectious load and its eventual neutralization signal the next phase of active anti-inflammation and proresolution ( ).

Citation: Bennett M, Gilroy D. 2017. Lipid Mediators in Inflammation, p 343-366. In Gordon S (ed), Myeloid Cells in Health and Disease. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.MCHD-0035-2016
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