The interplay between platelets and pathogenic bacteria (A11)

血小板和病原菌之间的相互作用 (A11)

• 批准号: 406445966
• 金额: --
• 依托单位: Abteilung Molekulare Genetik und Infektionsbiologie
• 依托单位国家: 德国
• 项目类别: CRC/Transregios
• 财政年份: 2018
• 资助国家: 德国
• 起止时间: 2017-12-31 至 2022-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/406445966?language=en
• 关键词: interplay; between; platelets; pathogenic; bacteria

Platelets and pathogenic bacteria mutually affect each other. Toxins from Streptococcus pneumoniae and Staphylococcus aureus can kill platelets, while platelet releasates impair S. aureus growth. Further, bacterial-derived platelet-activating proteins induce aggregation and thrombus formation, which immobilises bacteria but also causes tissue damage. We address the balance of these different effects. Ex vivo platelet receptors and induced signal cascades will be identified, and the interplay of bacteria and bacterial proteins with human megakaryocytes and the platelet-neutrophil axis will be analysed. In vivo we will decipher the impact of toxins and bacteria on platelets and neutrophils in a mouse pneumonia model and will test mechanisms of new therapeutic interventions.

血小板与致病菌相互影响。肺炎链球菌和金黄色葡萄球菌的毒素可以杀死血小板，而血小板的释放则损害了S。金黄色葡萄球菌生长此外，细菌衍生的血小板活化蛋白诱导聚集和血栓形成，其固定细菌但也引起组织损伤。我们解决这些不同影响的平衡。将鉴定离体血小板受体和诱导的信号级联，并分析细菌和细菌蛋白与人巨核细胞和血小板-中性粒细胞轴的相互作用。在体内，我们将在小鼠肺炎模型中破译毒素和细菌对血小板和中性粒细胞的影响，并将测试新的治疗干预机制。