Neutropenia induced by platelet-activating factor (PAF-acether) released from neutrophils: The inhibitory effect of prostacyclin (PGI2)

Camussi, Giovanni; Tetta, Ciro; Segoloni, Giuseppe; Deregibus, Maria Chiara; Bussolino, Federico

doi:10.1007/bf01978735

Cited by 31 publications

(12 citation statements)

References 14 publications

(1 reference statement)

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“…Platelets do not aggregate in vitro in the presence of chemotactic factors such as FMLP (personal observations). Recently, however, PMNLs have been shown to liberate PAF in the presence of chemotactic factors as well as during phagocytosis of immune complexes or microorganisms [5,28,29]. PAF is an extremely potent activator of platelet aggregation and secretion.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, Camussi et a1 [5] detected platelet-activating factor (PAF) in the circulation of rabbits within minutes of neutropenia and thrombocytopenia induced by C5, or FMLP infusion. This raised the possibility that PAF may be a second mediator responsible for the platelet response during C5a-or FMLP-induced neutropenia.…”

Section: Effect Of Infusion Of Platelet-activating Factor On Plateletmentioning

confidence: 99%

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The effect of intravascular neutrophil chemotactic factors on blood neutrophil and platelet kinetics

Issekutz

Ripley

1986

American J Hematol

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Intravenous infusion of an analogue (f-met-leu-phe [FMLP]) of a bacterial-derived polymorphonuclear leukocyte (PMNL) chemotactic factor, or of the complement-derived chemotactic stimulus, zymosan-activated plasma (ZAP, containing C5ades Arg) into rabbits induces acute PMNL margination in the pulmonary vasculature. This process also occurs during hemodialysis and the adult respiratory distress syndrome. The pulmonary PMNL sequestration is accompanied by thrombocytopenia. Because of the role platelets and PMNLs play in hemostasis and defense against infection, we studied the fate of these blood elements following sequestration induced by chemotactic factors. By employing 111In-labelled platelets and external radioisotope scanning, platelets were found to sequester in the pulmonary vasculature during FMLP infusion. Simultaneous 51Cr PMNL and 111In-platelet studies showed that following sequestration, PMNLs returned to the circulation and disappeared with a normal half-life (T1/2) whereas the T1/2 of the platelets was markedly shortened (T1/2 of control = 49 +/- 3.0 hr; FMLP or ZAP infused T1/2 = 27 +/- 2.7 hr). Infusion of platelet-activating factor (PAF) induced PMN and platelet sequestration with similar abnormalities in platelet kinetics. Studies with 51Cr- and 14C-serotonin-labelled platelets showed that platelets did not release serotonin during FMLP, ZAP, or low dose PAF-induced sequestration. In contrast to platelet survival, platelet size, platelet aggregation responses, and platelet glycoproteins were not affected by transient sequestration. These results indicate that during PMNL margination induced by relatively "pure" PMNL stimuli such as FMLP, platelets may reversibly marginate and subsequently be cleared at an accelerated rate. The reason for accelerated platelet clearance is not a result of circulating platelet aggregates or detectable proteolytic modification of membrane glycoproteins. Such altered platelet kinetics may contribute to thrombocytopenia during sepsis, the adult respiratory distress syndrome, and other states in which excess PMNL margination occurs.

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Section: Discussionmentioning

confidence: 99%

Section: Effect Of Infusion Of Platelet-activating Factor On Plateletmentioning

confidence: 99%

The effect of intravascular neutrophil chemotactic factors on blood neutrophil and platelet kinetics

Issekutz

Ripley

1986

American J Hematol

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“…Soluble and phagocytic stimuli have been reported to release PAF-aceter from granulo cytes [19] and might cause platelet aggrega tion during the incubation period, rendering the platelets refractory when tested photo metrically. PAF-aceter could not be assayed in our laboratory.…”

Section: Discussionmentioning

confidence: 99%

Effect of Latex-Stimulated Granulocytes on Platelet Aggregation in Man

Zoucas¹,

Fäldt

Ankerst

1985

Pathophysiol Haemos Thromb

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The effect of granulocytes on human platelet aggregation was investigated in vitro. Platelet function was assayed by photometric technique. Incubation of platelets with latex-stimulated granulocytes for 1 h at room temperature resulted in total inhibition of arachidonic acid-induced platelet aggregation. ADP-induced platelet aggregation was suppressed, lacked secondary wave and was pursued by swift disaggregation. Platelet aggregates induced by collagen dispersed faster under the influence of stimulated granulocytes. The present results indicate that granulocytes may play a role in the hemostatic mechanism in man.

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“…Since this type of hypotensive effect was brought about also by preparation M devoid of any PKA or kallikrein and with a very weak anticomplementary activity only, neither kinin generation nor complement activation was likely to be responsible for the phenomenon. Platelet activating factor has been described to mediate biological effects of immune complexes or aggregated IgG [12][13][14] and also to induce hypotension [15,16]. To …”

Section: Resultsmentioning

confidence: 99%

Hypotensive action of IgG preparations containing aggregates is suppressed by PAF-receptor antagonist BN 52021 and by gadolinium chloride (an agent blocking Kupffer cell function)

et al. 1991

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The hypotensive side effect of four IgG preparations was studied in a rat model. An unmodified, chromatographically isolated preparation (prepn. C) appeared to induce a transient drop in blood pressure via the kininogen kinin system. A preparation made by ethanol fractionation (prepn. E) and an ethanol-fractionated, modified product (prepn. M) produced an action which does not depend on kininogen activation. No blocking of kininase was required for this effect and it was brought about by prepn. M was devoid of any sizeable prekallikrein activator or kallikrein like proteinase content. The effect was associated by the aggregate fraction of prepn. E, but not with IgG monomers of the same preparation. Animals given these latter types of IgG preparations were refractory to a second dose 24 hours later. The involvement of PAF in the kinin-independent hypotensive action is suggested by the finding that PAF-receptor antagonist BN 52021 prevented the effect and returned the blood pressure close to normality when given during hypotension. A blockade of Kupffer cells brought about by administration of GdCl3 was also found to prevent the effect pointing to the involvement of these type of cells in the reactions.

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Neutropenia induced by platelet-activating factor (PAF-acether) released from neutrophils: The inhibitory effect of prostacyclin (PGI2)

Cited by 31 publications

References 14 publications

The effect of intravascular neutrophil chemotactic factors on blood neutrophil and platelet kinetics

The effect of intravascular neutrophil chemotactic factors on blood neutrophil and platelet kinetics

Effect of Latex-Stimulated Granulocytes on Platelet Aggregation in Man

Hypotensive action of IgG preparations containing aggregates is suppressed by PAF-receptor antagonist BN 52021 and by gadolinium chloride (an agent blocking Kupffer cell function)

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