LTB4 and PAF in the Cytokine Network

Plasmin-induced expression of cytokines and tissue factor in human monocytes involves AP-1 and IKKβ-mediated NF-κB activation

“…Although these data suggested a direct response to plasmin, indirect monocyte stimulation through autocrine loops were excluded in additional experiments. Thus, LTB 4 released by plasmin-stimulated monocytes 2,3 has been implicated in the augmentation of cytokine release from monocytes by some authors 41 but not by others. 42 Using 2 structurally different inhibitors of 5-lipoxygenase, zileuton, and MK-886, at concentrations that totally abolished plasmininduced formation of LTB 4 , we could show that this lipid mediator did not contribute to TNF-␣ expression (Syrovets et al, unpublished results, July 1998).…”

The pharmacogenetics of asthma: a candidate gene approach

“…Over the past 10 years, it has been shown that pharmacological inhibition of the action of ALOX5 or antagonism of the action of the cysteinyl leukotrienes at their receptor is associated with an amelioration of asthma. 64 Although a variety of biological actions have been ascribed to LTB 4 , it is predominantly a chemotactic moiety for eosinophils and neutrophils; 65,66 these actions occur via signal transduction at the LTB 4 receptors. 67 The cysteinyl leukotrienes were identified as a result of the search for the chemical structure of the materials that constituted the contractile activity known as slow-reacting sub-stance of anaphylaxis (SRS-A) 60,61 and are among the most potent bronchoconstrictor substances ever identified; 68,69 their actions result from signal transduction at the CysLT 1 receptor.…”

Aspirin-Triggered Lipoxin A4 and B4 Analogs Block Extracellular Signal-Regulated Kinase-Dependent TNF-α Secretion from Human T Cells

“…The key role of the classic eicosanoids, such as the prostanoids in the regulation of inflammatory and autoimmune disorders, is also well appreciated (4). In rheumatoid arthritis, which is mediated in part by the activation and recruitment of Ag-specific lymphocytes (5), leukotriene (LT) 3 B 4 generated locally can control T cell activation, regulating the inflammatory response (6,7).…”