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4. Thrombus formation induced by antibodies to beta2-glycoprotein I is complement dependent and requires a priming factor

Author

Valentina Pellis, Fabio Fischetti, Paolo Durigutto, Francesco Tedesco, Paolo Macor, Alessandra Debeus, Roberta Bulla, Daniele Sblattero, Pier Luigi Meroni, Fleur Bossi, Federica Ziller, Fischetti, Fabio, Durigutto, Paolo, Pellis, Valentina, Debeus, Alessandra, Macor, Paolo, Bulla, Roberta, Bossi, Fleur, Ziller, Federica, Sblattero, Daniele, Meroni, P., and Tedesco, Francesco

Subjects
Lipopolysaccharides, Male, Time Factors, Lipopolysaccharide, Fibrinogen, Biochemistry, Immunoglobulin G, chemistry.chemical_compound, immune system diseases, Medicine, Platelet, rat, Venous Thrombosis, biology, mesentery, Complement C5, Hematology, Complement C3, Antiphospholipid Syndrome, Complement C9, Trombus, Trombu, beta 2-Glycoprotein I, Antibodies, Antiphospholipid, Female, Antibody, medicine.drug, Immunology, Proinflammatory cytokine, Antiphospholipid syndrome, Escherichia coli, Animals, Humans, intravascular microscopy, Thrombus, Rats, Wistar, Blood Coagulation, Autoantibodies, Glycoproteins, Inflammation, business.industry, Thrombosis, Cell Biology, Complement System Proteins, medicine.disease, Protein Structure, Tertiary, Rats, chemistry, Microscopy, Fluorescence, biology.protein, Endothelium, Vascular, business
Abstract

We monitored the number of intravascular platelet-leukocyte aggregates (PLAs) and thrombotic occlusions (TOs) by intravascular microscopy in the mesentery of rats receiving antiphospholipid (aPL) immunoglobulin G (IgG) purified from the sera of patients with antiphospholipid syndrome. aPL IgG had no procoagulant effect, but it caused rapid endothelial deposition of fibrinogen, followed by PLA and TO in rats receiving an intraperitoneal injection of bacterial lipopolysaccharide 3 hours before IgG infusion. Anti-β2-glycoprotein I-depleted aPL IgG failed to induce PLAs and TOs. C3 and C9 colocalized with aPL IgG on the mesenteric vessels. The number of PLAs and TOs was markedly reduced in C6-deficient rats and in animals treated with anti-C5 miniantibody, suggesting the contribution of the terminal complement (C) complex to the aPL antibody-mediated intravascular thrombosis. In conclusion, our data indicate that antibodies to β2-glycoprotein I trigger coagulation subsequent to a priming proinflammatory factor and that the terminal C complex is the main mediator of the coagulation process.

Published
2005

5. Thrombus formation induced by antibodies to beta2-glycoprotein I is complement dependent and requires a priming factor.

Author

Fischetti F, Durigutto P, Pellis V, Debeus A, Macor P, Bulla R, Bossi F, Ziller F, Sblattero D, Meroni P, and Tedesco F

Subjects
Animals, Antibodies, Antiphospholipid immunology, Antiphospholipid Syndrome immunology, Antiphospholipid Syndrome metabolism, Autoantibodies chemistry, Blood Coagulation, Complement C3 metabolism, Complement C5 metabolism, Complement C9 metabolism, Complement System Proteins, Endothelium, Vascular cytology, Escherichia coli metabolism, Female, Fibrinogen chemistry, Fibrinogen metabolism, Glycoproteins chemistry, Humans, Immunoglobulin G chemistry, Inflammation, Lipopolysaccharides, Male, Microscopy, Fluorescence, Protein Structure, Tertiary, Rats, Rats, Wistar, Thrombosis blood, Time Factors, Venous Thrombosis blood, beta 2-Glycoprotein I, Glycoproteins immunology, Thrombosis metabolism
Abstract

We monitored the number of intravascular platelet-leukocyte aggregates (PLAs) and thrombotic occlusions (TOs) by intravascular microscopy in the mesentery of rats receiving antiphospholipid (aPL) immunoglobulin G (IgG) purified from the sera of patients with antiphospholipid syndrome. aPL IgG had no procoagulant effect, but it caused rapid endothelial deposition of fibrinogen, followed by PLA and TO in rats receiving an intraperitoneal injection of bacterial lipopolysaccharide 3 hours before IgG infusion. Anti-beta2-glycoprotein I-depleted aPL IgG failed to induce PLAs and TOs. C3 and C9 colocalized with aPL IgG on the mesenteric vessels. The number of PLAs and TOs was markedly reduced in C6-deficient rats and in animals treated with anti-C5 miniantibody, suggesting the contribution of the terminal complement (C) complex to the aPL antibody-mediated intravascular thrombosis. In conclusion, our data indicate that antibodies to beta2-glycoprotein I trigger coagulation subsequent to a priming proinflammatory factor and that the terminal C complex is the main mediator of the coagulation process.

Published
2005
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