The interplay between platelets and pathogenic bacteria (A11)

血小板和病原菌相互影响。肺炎链球菌和金黄色葡萄球菌的毒素可以杀死血小板，而释放的血小板则会阻碍金黄色葡萄球菌的生长。此外，细菌衍生的血小板激活蛋白会诱导聚集和血栓形成，这会使细菌固定，但也会造成组织损伤。我们解决了这些不同影响的平衡问题。将鉴定体外血小板受体和诱导的信号级联，并将分析细菌和细菌蛋白与人类巨核细胞和血小板-中性粒细胞轴的相互作用。在体内，我们将破译毒素和细菌对小鼠肺炎模型中血小板和中性粒细胞的影响，并将测试新的治疗干预措施的机制。

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.