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J Benveniste

Publications and source records attributed to J Benveniste.

At least 19 recordsLinked to original sources
PubMed1979

[Semi-synthesis and proposed structure of platelet-activating factor (P.A.F.): PAF-acether an alkyl ether analog of lysophosphatidylcholine].

We have studied the molecular structure of platelet-activating factor" (P.A.F.), a mediator of inflammation obtained from blood leukocytes, macrophages, and platelets themselves. We have semi-synthetized a substance that possesses all the known physicochemical and biological characteristics of P.A.F. from hog leukocytes. This was performed by successive methylation, hydrogenation, and acetylation of lysophosphatidylethanolamine plasmalogen. We therefore propose the following structure for P.A.F.: 1-0-alkyl-2-acetyl-glyceryl-3-phosphorylcholine. This molecular structure is not yet described among the numerous substances capable of inducing platelet aggregation and release.

Acetylation↗
PubMed1979

Platelet-activating factor and macrophages. I. Evidence for the release from rat and mouse peritoneal macrophages and not from mastocytes.

Platelet-activating factor (PAF) is a phospholipid mediator of anaphylaxis, released from basophils of several mammalian species, that aggregates platelets and releases their vasoactive amines. The ionophore A23 187 induced the release of PAF from rat and mouse peritoneal cells, a mixed cell population that was fractionated using 5--15% Ficoll gradients and adherence to plastic petri dishes. PAF was associated with large, acid phosphatase-containing, adherent mononuclear cells. Mastocytes did not release PAF but released histamine by the action of ionophore or 48/80; they could not be held responsible for inactivation of PAF or inhibition of the PAF-induced platelet aggregation. These data indicate that, besides blood basophils, peritoneal macrophages are a likely source for PAF, a result that adds a new important function to the macrophage:aggregation of platelets and liberation of their inflammatory and vasoactive substances.

Animals↗
PubMed1979

Platelet-lung in vivo interactions: an artifact of a multi-purpose model?

The simultaneous evaluation of platelet behaviour in vivo and of the accompanying bronchoconstriction in the guinea pig is described. Arachidonic acid induces bronchoconstriction, accompanied by, but independent from, thrombocytopenia, whereas collagen induces bronchoconstriction also accompanied by, but dependent from, thrombocytopenia. In both cases bronchoconstriction is due to cyclo-oxygenase metabolites of arachidonic acid. Use of potential inhibitors of thromboxane synthetase failed to reveal which of prostaglandin endoperoxides or thromboxane A2 is responsible for aspirin-inhibitive bronchoconstriction and thrombocytopenia. In contrast to PGE1 prostacyclin failed to interfere with bronchoconstriction by serotonin or by arachidonic acid, even though thrombocytopenia by the latter was suppressed. Bronchoconstriction by collagen, in contrast, was inhibited by nanogram doses of prostacyclin, confirming platelet-dependency. The combined bronchoconstriction/thrombocytopenia test in guinea pigs can discriminate sites of action of anti-inflammatory drugs, of agents which block specific platelet and/or bronchial receptors, which stimulate the cyclic AMP system, or generically which interfere with the mechanisms of bronchoconstriction and of thrombocytopenia.

Adenosine Diphosphate↗
PubMed1979

Circulating DNA:anti-DNA complexes in systemic lupus erythematosus. Detection and characterization by ultracentrifugation.

Although it is generally accepted that DNA:anti-DNA immune complexes play a significant role in the pathogenesis of tissue injury in systemic lupus erythematosus, their presence in the circulation is still a matter of controversy. In this study, we detected DNA:anti-DNA compexes by identification of both the antigen and(or) the antibody, the necessary requisites for immune complex definition, in 14 of 24 plasmas (7 of 11 patients). These antibodies were specific for native DNA and could be adsorbed by anti-immunoglobulin (Ig)G antisera. The DNA recovered was, at least in part, of low molecular weight. The presence of DNA:anti-DNA compexes was not related to high molecular weight IgG, cryoprecipitins, positive polyethylene glycol precipitation, or low plasma C3 levels. It was related significantly to low plasma C4 levels and to the presence of diffuse proliferative nephritis. The lack of correlation with other methods of detection of immune complexes and with the presence of heavy IgG (above 13 S) is in favor of the existence of other antigen-antibody systems (or aggregated immunoglobulins) in systemic lupus erythematosus plasmas. From the results, it appears that methods directed towards the demonstration of specific immune complexes are more informative than those detecting heavy or altered immunoglobulins.

Antigen-Antibody Complex↗
PubMed1978

[Macrophage origin of platelet activating factor].

Platelet-activating factor (P.A.F.) is a mediator of anaphylaxis released from human and Rabbit basophils which causes aggregation of platelets and release of their vasoactive amines. We have induced the release of P.A.F. from Rat peritoneal cells (P.C.) with ionophore A 23187. After fractionation of P.C. on 5-15% Ficoll gradients, P.A.F. was obtained from macrophage-rich but not from mastocyte-rich fractions and from adherent cells but not from non adherent cells. These data suggest an important new function for the macrophage: aggregation of platelets and release of their vasoactive amines and others mediators of inflammation.

Animals↗
PubMed1977

Detection of immediate hypersensitivity in rabbits by direct basophil degranulation.

The direct in vitro antigen-induced degranulation of rabbit basophils based on a simplified one-step method for the staining of these cells is reported. Degranulation was assessed by counting the number of basophils before and after exposure to antigen at 37 degrees C in the presence of Ca++. The degranulation was IgE-mediated, as shown by its passive transfer to nonimmunized rabbits by IgE-containing serum; also, the reaction was dependent on the presence of Ca++ ions and normal cell metabolism. The technique allowed the detection of serum factors capable of blocking the degranulation. It provided a means for following IgE sensitization at the cellular level, which is a better index of immediate hypersensitivity than the presence of circulating specific IgE.

Animals↗
PubMed1977

Release of platelet-activating factor and histamine. I. Effect of immune complexes, complement and neutrophils on human and rabbit mastocytes and basophils.

Immune complexes (ICs) triggered the degranulation of basophils/mastocytes in rabbit and man, thus releasing histamine and platelet-activating-factor. ICs acted upon basophils/mastocytes through complement activation and generation of anaphylatoxins and through release of cationic proteins from polymorphonuclear neutrophils. Anaphylatoxins and cationic proteins were active on human and rabbit mastocytes and on human basophils but not on rabbit basophils. Therefore, a cascade of cell to cell interactions may be envisaged implicating successively neutrophils, basophils and/or mastocytes and platelets. These interactions result in enhanced vascular permeability that allows ICs to be trapped along filtering basement membranes. This sequence could perpetuate the deposition of ICs, initially triggered by degranulation of basophils and mastocytes through the IgE-dependent mechanism, and furnish us with an explanation for the rather poorly understood involvement of platelets in immunopathology.

Anaphylatoxins↗
PubMed1976

Evidence for the involvement of IgE-basophil system in acute serum sickness.

The role of the basophils in acute serum sickness of rabbits was examined by monitoring daily the absolute number of basophils before, during and after the disease period. After antigen (bovine serum albumin, BSA) elimination, levels of serum IgE and in vitro basophil degranulation in the presence of BSA were determined. The results showed that the onset of glomerular lesions depends upon the simultaneous occurrence of circulating immune complexes greater than 19 S and of an in vivo basophil depletion--probably equivalent to degranulation--reaching 70% of the pre-disease number. Post-disease antigen-dependent in vitro degranulation of the basophils and levels of serum IgE anti BSA did not prove to be good indexes of basophil sensitization. Our data suggest that basophils are instrumental at early stages of the deposition of immune complexes, most probably through their sensitization by membrane-bound IgE antibodies.

Animals↗