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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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Submitted December 11, 2006
Accepted February 12, 2007
Platelet-bound lipopolysaccharide enhances Fc receptor-mediated phagocytosis of IgG opsonized platelets
John W. Semple*, Rukhsana Aslam, Michael Kim, Edwin R. Speck, and John Freedman
Department of Laboratory Medicine, St. Michael's Hospital, Toronto, Canada
Canadian Blood Services, Toronto, Canada
The Toronto Platelet Immunobiology Group, Toronto, Canada
Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada
* Corresponding author; email: semplej{at}smh.toronto.on.ca.
Platelets express toll-like receptor (TLR) 4 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=0.0001). 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 titres >4, there was a significant and synergistic increase in Fc-dependent platelet phagocytosis (p<0.0001, p=0.0031, p=0.0481 and p=0.0471) . These results suggest that, in the presence of anti-platelet 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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