Leukocyte-Dependent Histamine Release From Rabbit Platelets

Benveniste, Jacques; Henson, Peter M.; Cochrane, Charles G.

doi:10.1084/jem.136.6.1356

Cited by 1,174 publications

(267 citation statements)

References 24 publications

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“…Moreover, 5-HT released from aggregated platelets may cause bronchoconstriction manifested as wheezing in a patient with pulmonary embolism (109). It has been shown that 5-HT may be a potent mediator in the acute tracheal contraction elicited by platelet-activating factor (PAF) in dogs (85); PAF is a lipid mediator secreted during immune degranulation (7).…”

Section: Sources Of 5-ht Within the Pulmonary Systemmentioning

confidence: 99%

Effects of serotonin on airways: recent developments

Cazzola

D’Amato

et al. 1995

Allergy

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Serotonin (5-hydroxytryptamine, 5-HT) is an endogenous autacoid that can modulate activity in visceral sensory nerves. It produces complex physiologic actions within the cardiopulmonary system by interacting with both vascular and airway smooth-muscle 5-HT receptors (51). Although the role of 5-HT in humoral control of airway tone is not known, several interactions between this monoamine and the lung have been described. 5-HT is actively transported by the pulmonary endothelial cells where it is metabolized by monoamine oxidase, perhaps accounting for an affinity site on the outer layer of the mitochondria (112). Radio autographic localization has confirmed that pulmonary endothelial cells are the site of 5-HT uptake (112). Effects of 5-HT on airways5-HT is believed to have direct, complex indirect, or both actions on smooth muscle and nervous structures (51). The airway responses to 5-HT appear to be a summation of ongoing excitatory and inhibitory signals triggered or modified by this monoamine. A contractile response has been reported in airway muscle preparations from guinea pig, cat, dog, horse, cow, sheep, and calf (1,12,30,44,83,89, 108,117). No response is observed in the trachea and bronchus of rat, rabbit, and pig (27, 29), whereas a relaxation caused by 5-HT can be observed in goat trachea (28). Both in vivo and in vitro airway responses to 5-HT are often not as intense as to histamine or cholinergic agonists, may show tachyphylaxis, and may be partially or completely inhibited by pretreatment with atropine (62).5-HT causes constriction of both central and peripheral airways when given to vagotomized cats (34). However, the net effect of 5-HT infusion depends on the dose infused. Small amounts can induce air expulsion, while larger doses induce air retention because ofthe constriction ofthe large airways. Bronchoconstriction of large airways as well as of peripheral airways was observed in dogs during 5-HT perfusion by mechanical studies (38).The significance of 5-HT as a bronchoconstrictor in man remains to be determined. Experiments with tracheal muscle strips and bronchial spirals have shown that 5-HT causes weak contractions (10% of maximum) (37), although it can cause both constriction and relaxation of bronchioles and bronchi, depending on the concentration used (25,77,82). 5-HT causes relaxation when tone is induced in isolated human bronchial muscle preparations, an effect not blocked by 5-HT antagonists. In contrast, pulmonary vascular preparations always contract in 1

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Section: Sources Of 5-ht Within the Pulmonary Systemmentioning

confidence: 99%

Effects of serotonin on airways: recent developments

Cazzola

D’Amato

et al. 1995

Allergy

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“…Originally described as platelet activating factor (PAF), a soluble intermediate released following exposure of sensitized rabbit basophils to specific antigens (Benveniste, Henson & Cochrane, 1972), this active material is now known to be a series of phospholipids, 1-0-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine, and is referred to as AGEPC (Demopoulos, Pinckard & Hanahan, 1979,) or Pafacether (Benveniste, Tence, Varrene, Bidault, Boullet & Polonsky, 1979). Like many other materials released in allergic reactions, Paf-acether elicits inflammatory responses, as has been demonstrated in the skin (Stimler, Bloor, Hugli, Wykle, McCall & O'Flaherty, 1981;Wedmore & Williams, 1981a;Humphrey, McManus, Satouchi, Hanahan & Pinckard, 1982;Paul & Page, 1982) and paw (Bonnet, Loisseau, Orvoen & Bessin, 1981;Vargaftig & Ferreira, 1981;) of experimental animals and in the skin of man (Pinckard, Kniker, Lee, Hanahan & McManus, 1981;Basran, Page, Paul & Morley, 1983).…”

Section: Introductionmentioning

confidence: 99%

Inflammatory actions of platelet activating factor (Paf‐acether) in guinea‐pig skin

Morley¹,

Page²,

Paul³

1983

British J Pharmacology

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1Cutaneous responses to synthetic platelet activating factor (Paf-acether) have been studied in guinea-pigs by means of radioisotopic marker techniques. 2 Intradermal injection of Paf-acether elicited increased plasma protein extravasation (IPPE) (0.2-200 pmol/site), platelet accumulation (PA) (20-200 pmol/site) and red blood cell accumulation (RBCA) (200 pmol/site), whereas lyso-Paf (up to 2 nmol/site) was inactive in all these respects. 3 Following intradermal injection, the IPPE responses to Paf-acether (2 and 20 pmol/site) were complete within 15 and 30 min respectively, although in response to 200 pmol/site, IPPE was detectable up to 1.5 h. The PA and RBCA responses to Paf-acether (200 pmol/site) were complete within 1 h. 4 IPPE induced by Paf-acether (3 pmol/site) was potentiated by concomitant intradermal injection of a cutaneous vasodilator prostaglandin E2 (PGE2, lnmol/site) and inhibited by the Padrenoceptor agonist, isoprenaline (4.5 nmol/site) or the cx-adrenoceptor agonist, phenylephrine (6 nmol/site). Such observations are consistent with Paf-acether effecting increased vessel wall permeability. 5 Intradermal injection of PGE1 (3 nmol/site) significantly reduced PA in response to Paf-acether (200 pmol/site), whilst significantly enhancing IPPE. This dissociation of increased vascular permeability from PA is consistent with Paf-acether eliciting IPPE via a platelet-independent mechanism. 6 These results indicate that a direct effect on vessel wall permeability contributes to the inflammatory response to Paf-acether in guinea-pig skin. It is suggested that Paf-acether is a potential mediator of allergy and inflammation.

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“…PAF was initially recognized as a product of IgE-sensitized rabbit basophils (2) and was identified with 1-0-alkyl-2-sn-glyceryl-3-phosphorylcholine (3)(4)(5). It was subsequently shown that PAF is synthesized after appropriate stimulation by monocytes/macrophages (6)(7)(8)(9), polymorphonuclear neutrophils (7,10,11), platelets (12) and endothelial cells (13)(14)(15) .…”

mentioning

confidence: 99%

“…It was subsequently shown that PAF is synthesized after appropriate stimulation by monocytes/macrophages (6)(7)(8)(9), polymorphonuclear neutrophils (7,10,11), platelets (12) and endothelial cells (13)(14)(15) . PAF induces aggregation and degranulation of platelets (2,16), stimulates contraction of smooth muscle (17), promotes chemotaxis and granule secretion of neutrophils (18)(19) and monocytes (20), increases vascular permeability, and alters the vascular tone (21).…”

mentioning

confidence: 99%

Tumor necrosis factor/cachectin stimulates peritoneal macrophages, polymorphonuclear neutrophils, and vascular endothelial cells to synthesize and release platelet-activating factor.

Camussi

Bussolino

Salvidio

et al. 1987

The Journal of Experimental Medicine

340

133

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Platelet-activating factor (PAF)' is a mediator of inflammation with a wide range of biological activities (see reference 1 for review) . PAF was initially recognized as a product of IgE-sensitized rabbit basophils (2) and was identified with 1-0-alkyl-2-sn-glyceryl-3-phosphorylcholine (3-5). It was subsequently shown that PAF is synthesized after appropriate stimulation by monocytes/macrophages (6-9), polymorphonuclear neutrophils (7, 10, 11), platelets (12) and endothelial cells (13-15) . PAF induces aggregation and degranulation of platelets (2, 16), stimulates contraction of smooth muscle (17), promotes chemotaxis and granule secretion of neutrophils (18-19) and monocytes (20), increases vascular permeability, and alters the vascular tone (21).It was recently suggested that PAF is a mediator of endotoxic shock (22-24) on the basis of the following observations : (a) PAF is produced during endotoxic shock and experimental sepsis by Gram-negative bacteria (23-25) ; (b) infusion of experimental animals with PAF results in hypotension, decrease in cardiac output, and hypovolemic shock (26-28) ; (c) three PAF receptor antagonists (CV3988, kadsurenone, and SRI 63072) inhibit or reverse endotoxin-induced hypotension and, in this way, prolong the survival of rats (22,23,29) .Tumor necrosis factor/cachectin (TNF) is a mediator of endotoxic shock (30). Because TNF administration to experimental animals reproduces several aspects of PAF infusion (30), it seems possible that PAF is synthesized in response to

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Leukocyte-Dependent Histamine Release From Rabbit Platelets

Cited by 1,174 publications

References 24 publications

Effects of serotonin on airways: recent developments

Effects of serotonin on airways: recent developments

Inflammatory actions of platelet activating factor (Paf‐acether) in guinea‐pig skin

Tumor necrosis factor/cachectin stimulates peritoneal macrophages, polymorphonuclear neutrophils, and vascular endothelial cells to synthesize and release platelet-activating factor.

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