Thromboxane B2 (TxB2) release during IgE anaphylaxis in the rabbit

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Abstract

Intravenous antigen challenge of specifically IgE-sensitized rabbits resulted within 30 sec in significant elevations of plasma thromboxane B2 (TxB2) levels. Maximal TxB2 release (5 to 15 ng/ml) occurred within 120 to 180 sec after antigen challenge and was accompanied by the secretion of platelet factor 4 (PF4); however, PF4 release was delayed approximately 30 sec when compared to TxB2 release. Simultaneously, basopenia, thrombocytopenia, and neutropenia occurred within 30 sec after antigen challenge with maxiaml depression by 60 sec. Intraperitoneal administration of aspirin (acetyl salicylic acid, 100 mg/kg) 18 hr before antigen challenge did not prevent the development of thrombocytopenia, neutropenia, basopenia, or the release of PF4, but significantly reduced the release of TxB2. However, 7 of 10 aspirin-treated IgE rabbits died within 5 min after antigen challenge compared to no fatalities in 8 nonaspirin treated IgE rabbits. Since previous studies have demonstrated that platelet-activating factor (PAF) is released into the circulation during anaphylaxis, the dose-response characteristics of PAF-induced rabbit platelet secretion of serotonin and PF4 were compared to TxB2 production in vitro. Platelet synthesis of TxB2 was PAF dose dependent as was the secretion of serotonin and PF4; initial TxB2 synthesis (40 pg/ml) occurred at a PAF concentration that stimulated the release of 30% serotonin and 40 ng/ml PF4. The results of these in vivo and in vitro studies suggest that TxB2 release in the circulation during IgE-induced anaphylaxis in the rabbit may, in part, be due to PAF stimulation of thromboxane synthesis by circulating rabbit platelets; however, arachidonic acid metabolism through the cyclooxygenase pathway is not required for the alterations in circulating blood cells and platelet PF4 secretion and may, in fact, serve to attenuate the IgE anaphylactic syndrome.

Original languageEnglish (US)
Pages (from-to)1950-1954
Number of pages5
JournalJournal of Immunology
Volume125
Issue number5
StatePublished - 1980

Fingerprint

Thromboxane B2
Platelet Factor 4
Anaphylaxis
Immunoglobulin E
Platelet Activating Factor
Rabbits
Antigens
Blood Platelets
Serotonin
Neutropenia
Thrombocytopenia
Aspirin
Salicylic Acid
Thromboxanes
Prostaglandin-Endoperoxide Synthases
Arachidonic Acid
Blood Cells

ASJC Scopus subject areas

  • Immunology

Cite this

Thromboxane B2 (TxB2) release during IgE anaphylaxis in the rabbit. / Mcmanus, Linda M; Shaw, J. O.; Pinckard, R. N.

In: Journal of Immunology, Vol. 125, No. 5, 1980, p. 1950-1954.

Research output: Contribution to journalArticle

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abstract = "Intravenous antigen challenge of specifically IgE-sensitized rabbits resulted within 30 sec in significant elevations of plasma thromboxane B2 (TxB2) levels. Maximal TxB2 release (5 to 15 ng/ml) occurred within 120 to 180 sec after antigen challenge and was accompanied by the secretion of platelet factor 4 (PF4); however, PF4 release was delayed approximately 30 sec when compared to TxB2 release. Simultaneously, basopenia, thrombocytopenia, and neutropenia occurred within 30 sec after antigen challenge with maxiaml depression by 60 sec. Intraperitoneal administration of aspirin (acetyl salicylic acid, 100 mg/kg) 18 hr before antigen challenge did not prevent the development of thrombocytopenia, neutropenia, basopenia, or the release of PF4, but significantly reduced the release of TxB2. However, 7 of 10 aspirin-treated IgE rabbits died within 5 min after antigen challenge compared to no fatalities in 8 nonaspirin treated IgE rabbits. Since previous studies have demonstrated that platelet-activating factor (PAF) is released into the circulation during anaphylaxis, the dose-response characteristics of PAF-induced rabbit platelet secretion of serotonin and PF4 were compared to TxB2 production in vitro. Platelet synthesis of TxB2 was PAF dose dependent as was the secretion of serotonin and PF4; initial TxB2 synthesis (40 pg/ml) occurred at a PAF concentration that stimulated the release of 30{\%} serotonin and 40 ng/ml PF4. The results of these in vivo and in vitro studies suggest that TxB2 release in the circulation during IgE-induced anaphylaxis in the rabbit may, in part, be due to PAF stimulation of thromboxane synthesis by circulating rabbit platelets; however, arachidonic acid metabolism through the cyclooxygenase pathway is not required for the alterations in circulating blood cells and platelet PF4 secretion and may, in fact, serve to attenuate the IgE anaphylactic syndrome.",
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