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:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
通讯作者:
Worth RG
Worth RG
中科院分区:
其他
文献类型:
--
作者:
Ali RA;Wuescher LM;Dona KR;Worth RG

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血小板是止血的主要效应细胞。然而,最近的证据表明,血小板在宿主抵抗感染方面具有多种作用。我们和其他人的报告表明,血小板对金黄色葡萄球菌(S.aureus)感染具有保护作用。在目前的研究中,通过评估两种可能性来确定小鼠血小板参与宿主防御金黄色葡萄球菌感染的能力。首先,我们测定了血小板直接杀死金黄色葡萄球菌的能力;其次,我们测试了血小板增强巨噬细胞吞噬和细胞内杀灭金黄色葡萄球菌的可能性。我们在此报告支持这两种机制的证据。血小板有效地杀死了两种不同的金黄色葡萄球菌。临床分离的耐甲氧西林金黄色葡萄球菌(MRSA)可被血小板(2 h内杀灭40%)以凝血酶依赖的方式杀灭,而对甲氧西林敏感株(MSSA)的杀灭程度相同,但不需要凝血酶。有趣的是,凝血酶刺激的血小板也显著增强了MRSA和MSSA的腹膜巨噬细胞吞噬功能70%,并抑制了细胞内生长40%。增强巨噬细胞抗S。金黄色葡萄球菌的活动不依赖于与血小板的接触,但通过可释放的产物,即IL-1β介导。这些数据证实了我们的假设,即血小板通过直接杀死金黄色葡萄球菌和增强巨噬细胞的抗菌功能来参与宿主对金黄色葡萄球菌的防御。
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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