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1 Department of Surgery, Mayo Clinic Rochester, Rochester, Minnesota, United States; Physiology and Biomedical Engineering, Mayo Clinic Rochester, Rochester, Minnesota, United States
2 Department of Surgery, Mayo Clinic Rochester, Rochester, Minnesota, United States; Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic Rochester, Rochester, Minnesota, United States
3 Department of Medicine, Mayo Clinic Rochester, Rochester, Minnesota, United States
4 Biochemistry and Molecular Biology, Mayo Clinic Rochester, Rochester, Minnesota, United States
5 Biochemistry and Molecular Biology, Mayo Clinic Rochester, Rochester, Minnesota, United States; Section of Hematology, Mayo Clinic Rochester, Rochester, Minnesota, United States
* To whom correspondence should be addressed. E-mail: miller.virginia{at}mayo.edu.
Gram negative bacteria release lipopolysaccharides (LPS), which activate Toll-like-receptor-4 (TLR4) in the host initiating an inflammatory response to infection. Infection increases risk for thrombosis. Platelets contribute to defense from infection and to thrombosis. Experiments were designed to determine whether LPS, through TLR4 signaling, affects platelet phenotype. Platelet responses in wild type (WT) mice and mice that lack the TLR4 gene (dTLR4) were compared following a single non-lethal injection of LPS (0.2mg/kg/i.v.). Compared to WT mice, mice without TLR4 had fewer circulating platelets with lower RNA content and which were less responsive to thrombin activated expression of P-selectin but were equally sensitive to aggregation or ATP secretion. One week following the LPS injection, the time it takes for the circulating platelet pool to turnover, the number of circulating platelets, thrombin-induced expression of P-selectin and collagen-activated aggregation were increased comparably in both groups of mice. Therefore, the change of the platelet pool to an activated phenotype one week after a single exposure to LPS appears to arise from a process that is independent of TLR4. The persistence of the effect one week after the injection suggests that the changes reflect an action of LPS on megakaryocytes and their platelet progeny rather than on circulating platelets, which would have been cleared.
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