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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.
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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.
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