|
|
Blood, 1 June 2007, Vol. 109, No. 11, pp. 4803-4805.
Prepublished online as a Blood First Edition Paper on February 13, 2007; DOI 10.1182/blood-2006-12-062695.
 Previous Article | Table of Contents | Next Article 
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Brief Report
Platelet-bound lipopolysaccharide enhances Fc receptor–mediated phagocytosis of IgG-opsonized platelets
John W. Semple1,6,
Rukhsana Aslam5,6,
Michael Kim6,
Edwin R. Speck5,6, and
John Freedman1,3,6
1 Department of Laboratory Medicine, St Michael's Hospital, Toronto, ON, Canada;
Departments of 2 Pharmacology
3 Medicine, and
4 Laboratory Medicine and Pathobiology, University of Toronto, ON, Canada;
5 Canadian Blood Services;
6 The Toronto Platelet Immunobiology Group, ON, Canada
Platelets express Toll-like receptor 4 (TLR4), and this has been shown to be responsible for the thrombocytopenia induced by lipopolysaccharide (LPS) administration in vivo. We studied the role of LPS in mediating platelet phagocytosis by THP-1 cells in vitro by flow cytometry. Opsonization of platelets with an IgG monoclonal (W6/32) antibody or with IgG autoantibody-positive sera from patients with autoimmune thrombocytopenia (AITP) significantly enhanced platelet phagocytosis (P < .001). In contrast, platelet phagocytosis did not occur if platelets were bound with only LPS. If, however, the LPS-bound platelets were also opsonized with either W6/32 or autoantibody-positive sera with titers greater than 4, there was a significant and synergistic increase in Fc-dependent platelet phagocytosis (P < .001, P = .003, P = .048, and P = .047). These results suggest that, in the presence of antiplatelet antibodies, bacterial products can significantly alter platelet phagocytosis, and this may have relevance to how Gram-negative infections enhance platelet destruction in some patients with AITP.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
D. B. Cines, J. B. Bussel, H. A. Liebman, and E. T. Luning Prak
The ITP syndrome: pathogenic and clinical diversity
Blood,
June 25, 2009;
113(26):
6511 - 6521.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Zhang, J. Han, E. J. Welch, R. D. Ye, T. A. Voyno-Yasenetskaya, A. B. Malik, X. Du, and Z. Li
Lipopolysaccharide Stimulates Platelet Secretion and Potentiates Platelet Aggregation via TLR4/MyD88 and the cGMP-Dependent Protein Kinase Pathway
J. Immunol.,
June 15, 2009;
182(12):
7997 - 8004.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. Maugeri, P. Rovere-Querini, V. Evangelista, C. Covino, A. Capobianco, M. T. S. Bertilaccio, A. Piccoli, L. Totani, D. Cianflone, A. Maseri, et al.
Neutrophils phagocytose activated platelets in vivo: a phosphatidylserine, P-selectin, and {beta}2 integrin-dependent cell clearance program
Blood,
May 21, 2009;
113(21):
5254 - 5265.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
X.-L. Zhang, J. Peng, J.-Z. Sun, J.-J. Liu, C.-S. Guo, Z.-G. Wang, Y. Yu, Y. Shi, P. Qin, S.-G. Li, et al.
De novo induction of platelet-specific CD4+CD25+ regulatory T cells from CD4+CD25- cells in patients with idiopathic thrombocytopenic purpura
Blood,
March 12, 2009;
113(11):
2568 - 2577.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Stasi, A. Sarpatwari, J. B. Segal, J. Osborn, M. L. Evangelista, N. Cooper, D. Provan, A. Newland, S. Amadori, and J. B. Bussel
Effects of eradication of Helicobacter pylori infection in patients with immune thrombocytopenic purpura: a systematic review
Blood,
February 5, 2009;
113(6):
1231 - 1240.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Kjaersgaard, R. Aslam, M. Kim, E. R. Speck, J. Freedman, D. I. H. Stewart, E. J. Wiersma, and J. W. Semple
Epitope specificity and isotype of monoclonal anti-D antibodies dictate their ability to inhibit phagocytosis of opsonized platelets
Blood,
August 15, 2007;
110(4):
1359 - 1361.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
