Staphylococcus aureus lipoteichoic acid inhibits platelet activation and thrombus formation via the Paf receptorWaller, A. K., Sage, T., Kumar, C., Carr, T., Gibbins, J. M. ORCID: https://orcid.org/0000-0002-0372-5352 and Clarke, S. R. (2013) Staphylococcus aureus lipoteichoic acid inhibits platelet activation and thrombus formation via the Paf receptor. Journal of Infectious Diseases, 208 (12). pp. 2046-2057. ISSN 1537-6613
It is advisable to refer to the publisher's version if you intend to cite from this work. See Guidance on citing. To link to this item DOI: 10.1093/infdis/jit398 Abstract/SummaryImpaired healing is common in wounds infected with the major human pathogen Staphylococcus aureus, although the underlying mechanisms are poorly understood. Here, we show that S.aureus lipoteichoic acid (LTA) inhibits platelet aggregation caused by physiological agonists and S. aureus and reduced platelet thrombus formation in vitro. The presence of D-alanine on LTA is necessary for the full inhibitory effect. Inhibition of aggregation was blocked using a monoclonal anti-platelet activating factor receptor (PafR) antibody and Ginkgolide B, a well-defined PafR antagonist, demonstrating that the LTA inhibitory signal occurs via PafR. Using a cyclic AMP (cAMP) assay and a western blot for phosphorylated VASP, we determined that cAMP levels increase upon platelet incubation with LTA, an effect which inhibits platelet activation. This was blocked when platelets were preincubated with Ginkgolide B. Furthermore, LTA reduced haemostasis in a mouse tail-bleed assay.
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