Disease relevance of PAF acether

• These results suggest that alpha 1-PI prevents the proteolytic action and cell activation leading to PAF synthesis in peritonitis free patients [1].
• Hypoxia primes endotoxin-induced tissue factor expression in human monocytes and endothelial cells by a PAF-dependent mechanism [2].
• The purpose of this study was to examine the role of platelet-activating factor (PAF) in the development of PIB after allergic reaction [3].
• Ozone-induced pulmonary inflammation and epithelial proliferation are partially mediated by PAF [4].
• The effect of the selective PAF antagonist CIS-19 on PAF- and antigen-induced bronchoconstriction, microvascular leakage and bronchial hyperreactivity in guinea-pigs [5].

High impact information on PAF acether

• The latter appeared to be involved in the inhibition of proinflammatory cytokine production because addition of exogenous TGF-beta1, prostaglandin E2, or PAF resulted in inhibition of lipopolysaccharide-stimulated cytokine production [6].
• The objective of this study was to determine if the enhanced leukocyte adherence and emigration associated with inhibition of NO production involves inflammatory agents such as platelet-activating factor (PAF) and leukotriene B4 (LTB4) and/or phospholipase A2 (PLA2) [7].
• Spermine-NO prevented the mast cell-dependent neutrophil adhesion but failed to affect direct adhesion with PAF [8].
• Because of the structural similarities between PAF and the truncated phosphatidylcholines (polar PCs) generated during lipoprotein oxidation, we investigated the possibility that LCAT may also hydrolyze polar PCs to lyso-PC during the oxidation of plasma [9].
• We used eNOS-deficient (eNOS-/-) mice and their wild-type control as experimental animals, platelet-activating factor (PAF) at 10(-7) m as the test pro-inflammatory agent, and integrated optical intensity (IOI) as an index of microvascular permeability [10].

Chemical compound and disease context of PAF acether

• The results provide evidence of the coinvolvement of PAF, prostaglandins, histamine, and reactive oxygen radicals in dithranol-induced irritative dermatitis in mice [11].
• Release of arachidonic acid from membrane glycerophospholipids by cytosolic phospholipase A2 (cPLA2) is a key step in the generation of platelet-activating factor (PAF), recognized as the most proximal mediator of inflammatory events triggered by bacterial infection [12].
• Cotinine possibly increases the turnover rate of platelet-activating factor (PAF) because it is a potent activator of PAF hydrolase, and it may play a significant role in tobacco-induced arterial thrombosis [13].
• The production of PGI2 in PAECs was inhibited by hypoxia or verapamil, but promoted by angiotensin II (A II), noradrenaline (NE) or platelet activating factor (PAF), while that of TXA2 slightly increased except when treated with PAF [14].
• Effect of SRI 63-675 on hemodynamics and blood PAF levels during porcine endotoxemia [15].

Biological context of PAF acether

• 111In-eosinophil accumulation induced by PAF and in the PCA reaction was also inhibited by L-NAME but not by D-NAME.(ABSTRACT TRUNCATED AT 250 WORDS)[16]
• PAF has been proposed to be a retrograde messenger of long-term potentiation (LTP): the antagonist of PAFRs, ginkgolide B (or BN52021) prevents induction of LTP [17].
• Significant inhibition (45%) of PAF-release was obtained with 50 microM cloricromene and the IC50 was 85 microM [18].
• 3. I.v. administration of PAF induced a small accumulation of 111indium-labelled neutrophils within the pulmonary circulation which could be greatly potentiated by pretreatment of the animals with L-NAME [19].
• 4. The present findings indicate that inhibition of endogenous NO synthesis leads to an increase in protein extravasation and to potentiation of the permeability effects of PAF and endothelin-1 in the coronary circulation [20].

Anatomical context of PAF acether

• In addition to IFN-gamma, chemoattractant molecules, such as platelet-activating factor (PAF) and CC chemokines, may also activate macrophages to induce NO and mediate the killing of T. cruzi in an NO-dependent manner [21].
• Similarly, PAF increased IOI in the mesentery of wild-type mice but much less in the mesentery of eNOS-/- mice [10].
• 111In-labelled eosinophil accumulation induced by platelet-activating factor (PAF) and zymosan-activated plasma (as a source of C5a des Arg) was also inhibited [22].
• As a control we used plasma extravasation induced by platelet activating factor (PAF), which acts directly on the endothelium of the blood vessels, that is, its action is independent of any innervation [23].
• Incubation of EC with histamine or PAF for 1 h resulted in a four- to eight-fold decrease of beta-adrenoreceptor density in the plasma membranes [24].

Associations of PAF acether with other chemical compounds

• However, spermine NO did not directly inhibit histamine-induced leukocyte rolling and only partly affected PAF-induced leukocyte adhesion [8].
• Platelet-activating factor (PAF) receptor antagonist WEB 2086 also prevented the L-NAME-induced neutrophil adhesion [25].
• The effect of PMN priming by platelet-activating factor (PAF), and the effect of NAC on normal monocyte and on normal or hemodialysis patient's (N = 16) PMN oxidative responses were compared [26].
• RESULTS: The mean (+/- SEM) IOI of the control group was 8.7 +/- 5.2, whereas the group primed with PAF and histamine was 62.4 +/- 10 [27].
• 3. Co-administration of prostaglandin E2 (PGE2), prostaglandin I2 (PGI2), calcitonin gene-related peptide (CGRP), 5-hydroxytryptamine (5-HT), substance P (SP) or platelet activating factor (PAF) (1 pmol-1 nmol/paw) with BK (1 nmol/paw) dose-dependently potentiated BK-induced paw oedema [28].

Gene context of PAF acether

• Previous studies of crystal structures of GM2AP complexed with the physiological ligand GM2 and platelet activating factor (PAF) have shown binding at two specific locations within the spacious apolar pocket and an ordering effect of endogenous resident lipids [29].
• The induction of iNOS is mediated by the release of endogenous tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), and PAF by endotoxin [30].
• In the earlier phases of shock, activation of the endothelial, constitutive NOS (ecNOS) occurs, which, in the case of endotoxic shock, is triggered by endotoxin-induced, acute release of platelet-activating factor (PAF) and also other potential mediators [30].
• In alpha-toxin-permeabilized PMNs, AA release and PAF production result from the specific activation of cytosolic PLA2 (cPLA2) [31].
• PAF increased IOI to comparable values in the mesenteries of wild-type mice and those lacking the gene for inducible NOS (iNOS) [10].

Analytical, diagnostic and therapeutic context of PAF acether

• Perfusion with PAF (10 nM) induced a robust transient high Lp [24.3 +/- 1.7 x 10-7 cm/(s.cmH2O)] that peaked in 8.9 +/- 0.5 min and then returned toward control Lp [1.6 +/- 0.1 x 10-7 cm/(s.cmH2O)] [32].
• Reconstruction of venular segments with the use of transmission electron microscopy of serial sections confirmed that PAF induces paracellular inflammatory gaps [32].
• 5. Electrical stimulation of the lumbar sympathetic chain at frequencies of 0.25-5 Hz, which probably also significantly decreases blood flow through the joint capsule, reduced basal plasma extravasation, BK-induced PE and PAF-induced PE [23].
• In conclusion, PGE2 and PAF, and ligation of VnR as well, contribute to amplify viral growth in HIV-1-infected macrophages upon uptake of apoptotic cells [33].
• The stimulation of cyclic GMP synthesis induced by PAF was dose-dependent and was suppressed after treatment with PCA-4248, a PAF antagonist, a fact that could suggest the involvement of specific PAF receptors [34].

References