Pyong Kyun Shin1, Konstantinos Konstantopoulos2, and Julia M. Ross1. (1) Chemical and Biochemical Engineering, UMBC, 1000 Hilltop Circle, Baltimore, MD 21250, (2) Chemical & Biomolecular Engineering, Johns Hopkins University, 3400 N. Charles Street, Maryland Hall Room 223, Baltimore, MD 21218
S. aureus infection begins when bacterial cells circulating in blood adhere to components of the extracellular matrix or endothelial cells of the host and initiate colonization. S. aureus binding to activated platelets may represent a key step in spreading of infection. Prior work has shown that red blood cells (RBCs) potentiate platelet aggregation through ADP secretion (chemical effect) and change of collision mode (physical effect). Here we investigate how RBCs modulate the adhesion of S. aureus to platelets in shear flow. The presence of RBCs drastically increases the adhesion of S. aureus to platelets at moderate shear rate (2000 s-1), whereas smaller changes are detected at low (100 s-1) and high (5000 s-1) shear rates. The adhesion levels increase with RBC concentration and reach maximal values at the physiological ratio of RBC to platelet (15:1). Conversion of ADP to ATP by creatine phosphokinase abolishes S. aureus binding to platelets at all shear rates, indicating that ADP plays a critical role in this process. RBCs markedly enhance the level of secreted ADP in sheared specimens which correlates with the increased platelet activation in the presence of RBC. The extent of S. aureus binding to platelets in the presence of either intact RBCs or RBC ghosts are somewhat comparable suggesting that ADP secretion from platelets and RBCs is not the sole factor contributing to the enhanced S. aureus - platelet adhesion. In this presentation, both chemical and physical effects of RBCs on the adhesion of S. aureus to platelets and will be discussed