Mechanisms of platelet-activating factor (PAF)-mediated responses in the lung.
Platelet-activating factor (PAF) is a potent lipid mediator that has been implicated in asthma, sepsis, acute lung injury and ischemia/reperfusion injury. Its actions in the lungs include vasoconstriction, bronchoconstriction, and edema formation. Despite the fact that PAF exerts these actions within minutes, they are mediated by other lipid mediators, in particular eicosanoids generated by cyclooxygenase and lipoxygenase enzymes and sphingolipids generated by acid sphingomyelinase.We will discuss the mechanisms of the PAF-induced pressor responses that are triggered by thromboxane A(2) and leukotrienes, as well the PAF-induced increase in vascular permeability that is mediated by prostaglandin E(2) (PGE(2)) and ceramide.
Uhlig
Stefan
S
Division Pulmonary Pharmacology, Research Center Borstel, Leibniz-Center for Medicine and Biosciences, Parkallee 22, 23845 Borstel, Germany. suhlig@fz-borstel.de
Göggel
Rolf
R
Engel
Stephanie
S
D000818:Animals; D002518:Ceramides / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism; D006801:Humans; D015289:Leukotrienes / Q000378:metabolism; D008168:Lung / Q000503:physiopathology*; D010539:Permeability; D010972:Platelet Activating Factor / Q000378:metabolism*; D013928:Thromboxane A2 / Q000378:metabolism
D002518:Ceramides; D015289:Leukotrienes; D010972:Platelet Activating Factor; D013928:Thromboxane A2; D015232:Dinoprostone