作者: Amie K. Waller , Tanya Sage , Christopher Kumar , Thomas Carr , Jonathan M. Gibbins
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摘要: Impaired healing is common in wounds infected with the major human pathogen Staphylococcus aureus, although underlying mechanisms are poorly understood. Here, we show that S. aureus lipoteichoic acid (LTA) inhibits platelet aggregation caused by physiological agonists and reduced thrombus formation vitro. The presence of D-alanine on LTA necessary for full inhibitory effect. Inhibition was blocked using a monoclonal anti-platelet activating factor receptor (PafR) antibody Ginkgolide B, well-defined PafR antagonist, demonstrating signal occurs via PafR. Using cyclic AMP (cAMP) assay Western blot phosphorylated VASP, determined cAMP levels increase upon incubation LTA, an effect which activation. This when platelets were preincubated B. Furthermore, hemostasis mouse tail-bleed assay.