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Platelet-Activating Factor (PAF) in Infectious Diseases

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Bioactive Lipid Mediators
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Abstract

Platelet-activating factor (PAF) is a phospholipid that was originally discovered as an IgE-sensitized rabbit basophil-derived substance responsible for platelet aggregation. The chemical structure was determined to be 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine. The cellular effects of PAF are mediated by a specific G protein-coupled receptor (PAFR). When PAF is administered to laboratory animals, versatile pharmacological responses including platelet aggregation occur. In some studies, the pathophysiological roles of PAF have been deduced from observations that PAF production and PAFR expression are increased in the affected tissues or organs. Furthermore, mimicking of pathophysiological conditions by PAF and suppressive effects of PAF antagonists also suggest significant roles for PAF in some diseases. Under such experimental circumstances, PAFR-knockout (KO) mice were first reported in 1998. Since then, numerous studies using PAFR-KO mice have provided insight into multiple pathophysiological roles of PAF. Some of the studies used experimental infection models with various pathogens. This chapter reviews the current understanding of the PAF/PAFR axis and its protective or deleterious roles in infectious diseases.

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Ishii, S. (2015). Platelet-Activating Factor (PAF) in Infectious Diseases. In: Yokomizo, T., Murakami, M. (eds) Bioactive Lipid Mediators. Springer, Tokyo. https://doi.org/10.1007/978-4-431-55669-5_7

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