Background:

PAF C-16 is a naturally occurring phospholipid produced upon stimulation through two distinct pathways known as the “remodeling” and 'de novo' pathways.[1] It is a potent mediator of neutrophil migration,[2] and the production of reactive oxygen species, and IL-6 in human macrophages.[3],[4] It is a more potent mediator of platelet aggregation than PAF C-18.[5] Pathological processes involving PAF include necrotizing enterocolitis,[6] inflammation, asthma, and allergy.[7]

Reference:
[1]. Prescott, S.M., Zimmerman, G.A., and McIntyre, T.M. Platelet-activating factor. The Journal of Biological Chemisty 265, 17381-17384 (1990).
[2]. Carolan, E.J., and Casale, T.B. Degree of platelet activating factor-induced neutrophil migration is dependent upon the molecular species. Journal of Immunology 145, 2561-2565 (1990).
[3]. Rouis, M., Nigon, F., and Chapman, M.J. Platelet activating factor is a potent stimulant of the production of active oxygen species by human monocyte-derived macrophages. Biochemical and Biophysical Research Communications 156, 1293-1301 (1988).
[4]. Thivierge, M., and Rola-Pleszczynski, M. Platelet-activating factor enhances interleukin-6 production by alveolar macrophages. Journal of Allergy and Clinical Immunology 90, 796-802 (1992).
[5]. Stewart, A.G., and Grigoriadis, G. Structure-activity relationships for platelet-activating factor (PAF) and analogs reveal differences between PAF receptors on platelets and macrophages. Journal of Lipid Mediators 4, 299-308 (1991).
[6]. Wang, H., Tan, X.D., Qu, X.W., et al. Platelet-activating factor (PAF) up-regulates plasma and tissue PAF-acetylhydrolase activity in the rat: Effect of cycloheximide. Pediatric Research 42, 597-603 (1997).
[7]. Sturk, A., Wouter Ten Cate, J., Hosford, D., et al. The synthesis, catabolism, and pathophysiological role of platelet-activating factor. Advances in Lipid Research 23, 219-276 (1989).