Platelets Mediate Host Defense against Staphylococcus aureus through Direct Bactericidal Activity and by Enhancing Macrophage Activities.
Platelets Mediate Host Defense against Staphylococcus aureus through Direct Bactericidal Activity and by Enhancing Macrophage Activities.
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DOI:
10.4049/jimmunol.1601178
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发表时间:
2017-01-01
期刊:
影响因子:
--
通讯作者:
Worth RG
中科院分区:
文献类型:
--
作者:
Ali RA;Wuescher LM;Dona KR;Worth RG
Platelets are the chief effector cells in hemostasis. However, recent evidence suggests that platelets have multiple roles in host defense against infection. Reports by us and others showed that platelets functionally contribute to protection against Staphylococcus aureus (S. aureus) infection. In the current study, the capacity of mouse platelets to participate in host defense against S. aureus infection was determined by assessing two possibilities. First, we determined the ability of platelets to kill S. aureus directly; and second, we tested the possibility that platelets enhance macrophage phagocytosis and intracellular killing of S. aureus. We report here evidence in support of both mechanisms. Platelets effectively killed two different strains of S. aureus. A clinical isolate of methicillin resistant S. aureus (MRSA) was killed by platelets (>40% killing in 2 h) in a thrombin-dependent manner while a methicillin sensitive strain (MSSA) was killed to equal extent but did not require thrombin. Interestingly, thrombin-stimulated platelets also significantly enhanced peritoneal macrophage phagocytosis of both MRSA and MSSA by >70%, and restricted intracellular growth by >40%. Enhancement of macrophage anti-S. aureus activities is independent of contact with platelets but is mediated through releasable products, namely IL-1β. These data confirm our hypothesis that platelets participate in host defense against S. aureus both through direct killing of S. aureus and enhancing the antimicrobial function of macrophages in protection against S. aureus infection.
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