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Arachidonate remodeling and PAF synthesis in human neutrophils

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Arachidonate Remodeling and Inflammation

Part of the book series: Progress in Inflammation Research ((PIR))

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Abstract

Both AA-derived eicosanoids and platelet activating factor (PAF) serve important physiological functions, but also participate in pathological developments [14]. The metabolism and actions of PAF, arachidonic acid (AA), and AA-derived eicosanoids are closely linked in neutrophils, indeed they can be derived from the same phospholipid precursor, 1-O-alkyl-2-AA-GPC (sn-glycero-3-phosphocholine). Neutrophils play a major role in host defense and inflammation and many studies have focused on neutrophil signaling systems and pharmacological intervention in these systems. Since neutrophils are terminally differentiated cells and can be maintained for only short periods of time after their isolation, molecular approaches for their study have been limited. In addition, many of the enzymes that are responsible for PAF and AA metabolism, except for cPLA2 (85 kDa cytosolic phospholipase A2) and 5-lipoxygenase, are membrane proteins and have not been isolated. Thus much of our knowledge of the lipid metabolism and lipid-mediated signaling has been obtained through the study of crude systems and intact cells. This review attempts to summarize the work of my colleagues and me in this area and closely related work of others. Our understanding of neutrophil signaling draws on numerous studies of other cells and tissues largely beyond the scope of this review but generally acknowledged in the primary literature cited.

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Wykle, R.L. (2004). Arachidonate remodeling and PAF synthesis in human neutrophils. In: Fonteh, A.N., Wykle, R.L. (eds) Arachidonate Remodeling and Inflammation. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-7848-7_5

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  • DOI: https://doi.org/10.1007/978-3-0348-7848-7_5

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