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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Mcdonald, P. P. Braquet, P. Borgeat, P. Mccoll, S. R. |
| Description | Author Affiliation: McDonald PP ( Centre de recherche en Inflammation, immunologie et rhumatologie, Institut de recherche du CHUL, Ste-Foy, Québec, Canada.) |
| Abstract | 1. Platelet-activating factor (PAF) and leukotriene B4 (LTB4), two potent lipid mediators synthesized by activated neutrophils, are known to stimulate several neutrophil functional responses. In this study, we have determined that endogenous LTB4 and PAF exert autocrine effects on LT synthesis, as well as the underlying mechanism involved. 2. Pretreatment of neutrophils with either pertussis toxin (PT), or with receptor antagonists for LTB4 and PAF, resulted in an inhibition of LT synthesis induced by calcium ionophore, A23187. This inhibition was most marked at submaximal (100-300 nM) A23187 concentrations, whilst it was least at ionophore concentrations which induce maximal LT synthesis (1-3 microM). Thus newly-synthesized PAF and LTB4 can enhance LT synthesis induced by A23187 under conditions where the LT-generating system is not fully activated. 3. In recombinant human (rh) granulocyte-macrophage colony-stimulating factor (GM-CSF)-primed neutrophils, LT synthesis in response to chemoattractants (fMet-Leu-Phe or rhC5a) was also significantly inhibited by the LTB4 receptor antagonist, and to a lesser extent by PAF receptor antagonists. 4. Further investigation revealed that LTB4 and/or PAF exert their effects on LT synthesis via an effect on arachidonic acid (AA) availability, as opposed to 5-lipoxygenase (5-LO) activation. Indeed, the receptor antagonists, as well as PT, inhibited LT synthesis and AA release to a similar extent, whereas 5-LO activation (assessed with an exogenous 5-LO substrate) was virtually unaffected under the same conditions. Accordingly, we showed that addition of exogenous LTB4 could enhance AA availability in response to chemoattractant challenge in rhGM-CSF-primed cells, without significantly affecting the 5-LO activation status. Our data show that newly-generated PAF and LTB4 have the ability to positively feedback on LT synthesis by acting at the level of the phospholipase A2/re-esterification component of the LT biosynthetic pathway in neutrophils. Such autocrine affects are likely to represent an important amplification step of LT synthesis, and may as such contribute to the rapid onset, as well as to the evolution, of inflammatory responses. |
| ISSN | 00071188 |
| e-ISSN | 14765381 |
| Journal | British Journal of Pharmacology |
| Issue Number | 3 |
| Volume Number | 111 |
| Language | English |
| Publisher | Wiley Online Library(on behalf of The British Pharmacological Society) |
| Publisher Date | 1994-03-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Leukotriene B4 Physiology Leukotrienes Biosynthesis Neutrophils Metabolism Platelet Activating Factor Amino Acid Sequence Arachidonate 5-Lipoxygenase Arachidonic Acid Secretion Calcimycin Pharmacology Complement C5a Enzyme Activation Granulocyte-Macrophage Colony-Stimulating Factor Molecular Sequence Data N-Formylmethionine Leucyl-Phenylalanine Pertussis Toxin Recombinant Proteins Signal Transduction Drug Effects Virulence Factors, Bordetella Research Support, Non-U.S. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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