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Merck
  • Platelet activation by Streptococcus pyogenes leads to entrapment in platelet aggregates, from which bacteria subsequently escape.

Platelet activation by Streptococcus pyogenes leads to entrapment in platelet aggregates, from which bacteria subsequently escape.

Infection and immunity (2014-07-30)
Lisbeth Svensson, Maria Baumgarten, Matthias Mörgelin, Oonagh Shannon
초록

Platelet activation and aggregation have been reported to occur in response to a number of Gram-positive pathogens. Here, we show that platelet aggregates induced by Streptococcus pyogenes were unstable and that viable bacteria escaped from the aggregates over time. This was not due to differential activation in response to the bacteria compared with physiological activators. All the bacterial isolates induced significant platelet activation, including integrin activation and alpha and dense-granule release, at levels equivalent to those induced by potent physiological platelet activators that induced stable aggregates. The ability to escape the aggregates and to resist the antibacterial effects of platelets was dependent on active protein synthesis by the bacteria within the aggregate. We conclude that S. pyogenes bacteria can temporarily cover themselves with activated platelets, and we propose that this may facilitate survival of the bacteria in the presence of platelets.

MATERIALS
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브랜드
제품 설명

Sigma-Aldrich
Prostaglandin E1, synthetic, powder, BioReagent, suitable for cell culture
Sigma-Aldrich
Prostaglandin E1, γ-irradiated, powder, BioXtra, suitable for cell culture
Sigma-Aldrich
Prostaglandin E1, ≥98% (HPLC), synthetic
Alprostadil, European Pharmacopoeia (EP) Reference Standard