Toll-like receptor and antiphospholipid mediated thrombosis: in vivo studies.

Toll-like receptor and antiphospholipid mediated thrombosis: in vivo studies. Research Abstract Details 

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Toll-like receptor and antiphospholipid mediated thrombosis: in vivo studies. Abstract Text:

Silvia S Pierangeli,Mariano E Vega-Ostertag,Elena Raschi,Xiaowei Liu,Zurina Romay-Penabad,Valeria De Micheli,Monica Galli,Marco Moia,Angela Tincani,Maria Orietta Borghi,Tracy Nguyen-Oghalai,Pier Luigi Meroni,

OBJECTIVE: A study was undertaken to investigate the in vivo pathogenic role of Toll-like receptor 4 (TLR-4) in the antiphospholipid syndrome (APS) by studying the thrombogenic antiphospholipid (aPL) activity in lipopolysaccharide (LPS) non-responsive (LPS-/-) mice and the association between tlr4 gene polymorphisms and APS in patients. METHODS: IgGs from two patients with APS, one with aPL negative systemic lupus erythematosus (SLE) and one with normal human serum (NHS), were evaluated for thrombosis, tissue factor (TF) activity and endothelial cell activation in LPS-/- mice displaying a tlr4 spontaneous mutation vs LPS responsive (LPS+/+) mice. Human tlr4 Asp299Gly and Thr399Ile polymorphisms were evaluated by allele-specific PCR in 110 patients with APS with arterial/venous thrombosis and in 220 controls of the same ethnic origin. RESULTS: IgG-APS produced significantly larger thrombi and more leucocytes (WBC) adhering to endothelial cells in the cremaster muscle microcirculation of LPS+/+ mice than IgG-NHS or aPL negative SLE-IgG. These effects were abrogated after absorption of the anti-beta(2)glycoprotein I activity by an affinity column. The two IgG-APS induced significantly smaller thrombi and fewer WBC adhering to endothelial cells in LPS-/- mice than in LPS+/+ mice. IgG-APS induced higher TF activity in carotid artery homogenates of LPS+/+ mice than in LPS-/- mice. The prevalence of Asp299Gly and Thr399Ile tlr4 polymorphisms was significantly lower than in controls. CONCLUSIONS: These findings in LPS-/- mice and the reduction in the "protective" polymorphism in patients with APS with thrombosis suggest that TLR-4 is involved in the interaction of aPL with endothelial cells in vivo.

Toll-like receptor and antiphospholipid mediated thrombosis: in vivo studies. Publishing Authors By Initials

SS Pierangeli,ME Vega-Ostertag,E Raschi,X Liu,Z Romay-Penabad,V De Micheli,M Galli,M Moia,A Tincani,MO Borghi,T Nguyen-Oghalai,PL Meroni,

For similar proteins: blood proteins: beta 2-glycoprotein i research abstracts see: proteins: blood proteins: beta 2-glycoprotein i research

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Toll-like receptor and antiphospholipid mediated thrombosis: in vivo studies. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Annals of the rheumatic diseases

VOLUME: 66

Page Numbers: 1327-33

Journal Abbreviation: Ann. Rheum. Dis.

ISSN: 0003-4967

DAY: 29

MONTH: 01

YEAR: 2007

Toll-like receptor and antiphospholipid mediated thrombosis: in vivo studies. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 372355

Toll-like receptor and antiphospholipid mediated thrombosis: in vivo studies. Keywords Mesh Terms:

KEYWORDS: beta 2-Glycoprotein I

MESH TERMS: immunology

Chemical & Substance for Abstract: Toll-like receptor and antiphospholipid mediated thrombosis: in vivo studies. Information

Substance Name: Thromboplastin

Registry Number: 9035-58-9

Grant and Affiliation Information for Toll-like receptor and antiphospholipid mediated thrombosis: in vivo studies.

AFFILIATION: Antiphospholipid Standardization Laboratory, Division of Rheumatology, Department of Internal Medicine, University of Texas Medical Branch, Galveston, Texas 77555-1165, USA. sspieran@utmb.edu

Country: England

AGENCY: United States PHS

GRANT: S02GMM08248

ACRONYM: RR

MEDLINETA: Ann Rheum Dis

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