Department of Medical Microbiology and Immunology, University of Toledo College of Medicine and Life Sciences, Toledo, Ohio, USA.
Department of Medical Microbiology and Immunology, University of Toledo College of Medicine and Life Sciences, Toledo, Ohio, USA
Infect Immun. 2018 Aug 22;86(9). doi: 10.1128/IAI.00186-18. Print 2018 Sep.
is a major human pathogen that can cause mild to severe life-threatening infections in many tissues and organs. Platelets are known to participate in protection against by direct killing and by enhancing the activities of neutrophils and macrophages in clearing infection. Platelets have also been shown to induce monocyte differentiation into dendritic cells and to enhance activation of dendritic cells. Therefore, in the present study, we explored the role of platelets in enhancing bone marrow-derived dendritic cell (BMDC) function against We observed a significant increase in dendritic cell phagocytosis and intracellular killing of a methicillin-resistant (MRSA) strain (USA300) by thrombin-activated platelets or their releasates. Enhancement of bacterial uptake and killing by DCs is mediated by platelet-derived CD40L. Coculture of USA300 and BMDCs in the presence of thrombin-activated platelet releasates invokes upregulation of the maturation marker CD80 on DCs and enhanced production of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin 12 (IL-12), and IL-6. Overall, these observations support our hypothesis that platelets play a critical role in the host defense against infection. Platelets stimulate DCs, leading to direct killing of and enhanced DC maturation, potentially leading to adaptive immune responses against .
金黄色葡萄球菌是一种重要的人类病原体，可导致许多组织和器官发生从轻度到危及生命的严重感染。已知血小板通过直接杀伤和增强中性粒细胞和巨噬细胞清除金黄色葡萄球菌感染的活性来参与保护。血小板还被证明可以诱导单核细胞分化为树突状细胞，并增强树突状细胞的激活。因此，在本研究中，我们探讨了血小板在增强骨髓来源的树突状细胞（BMDC）对抗金黄色葡萄球菌功能中的作用。我们观察到，凝血酶激活的血小板或其释放物显著增加了树突状细胞对耐甲氧西林金黄色葡萄球菌（MRSA）菌株（USA300）的吞噬作用和细胞内杀伤作用。DC 摄取和杀伤能力的增强是由血小板衍生的 CD40L 介导的。在凝血酶激活血小板释放物存在的情况下，USA300 与 BMDC 共培养会引起 DC 上成熟标志物 CD80 的上调，并增强促炎细胞因子肿瘤坏死因子-α（TNF-α）、白细胞介素 12（IL-12）和 IL-6 的产生。总的来说，这些观察结果支持我们的假设，即血小板在宿主防御金黄色葡萄球菌感染中发挥关键作用。血小板刺激树突状细胞，导致金黄色葡萄球菌的直接杀伤和树突状细胞的成熟增强，可能导致针对金黄色葡萄球菌的适应性免疫反应。
