Platelet activation by Streptococcus pyogenes leads to entrapment in platelet aggregates from which bacteria subsequently escape.
(2014) In Infection and Immunity 82(10). p.4307-4314- Abstract
- Platelet activation and aggregation has 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 viable bacteria escaped from the aggregates over time. This was not due to a differential activation in response to the bacteria as compared with physiological activators. All the bacteria isolates induced significant platelet activation, including integrin activation, alpha and dense granule release, at equivalent levels to potent physiological platelet activators that induced stable aggregates. The ability to escape the aggregates and resist antibacterial effects of platelets was dependent on active protein synthesis by the bacteria... (More)
- Platelet activation and aggregation has 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 viable bacteria escaped from the aggregates over time. This was not due to a differential activation in response to the bacteria as compared with physiological activators. All the bacteria isolates induced significant platelet activation, including integrin activation, alpha and dense granule release, at equivalent levels to potent physiological platelet activators that induced stable aggregates. The ability to escape the aggregates and resist antibacterial effects of platelets was dependent on active protein synthesis by the bacteria within the aggregate. We conclude that S. pyogenes can temporarily cover themselves with activated platelets and we propose that this may facilitate survival of bacteria in the presence of platelets. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4581199
- author
- Svensson, Lisbeth LU ; Baumgarten, Maria LU ; Mörgelin, Matthias LU and Shannon, Oonagh LU
- organization
- publishing date
- 2014
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Infection and Immunity
- volume
- 82
- issue
- 10
- pages
- 4307 - 4314
- publisher
- American Society for Microbiology
- external identifiers
-
- pmid:25069984
- wos:000341935100029
- scopus:84907091624
- pmid:25069984
- ISSN
- 1098-5522
- DOI
- 10.1128/IAI.02020-14
- language
- English
- LU publication?
- yes
- id
- 11516055-b083-487d-ade4-e7b301562bb7 (old id 4581199)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/25069984?dopt=Abstract
- date added to LUP
- 2016-04-01 10:38:49
- date last changed
- 2022-03-12 07:43:06
@article{11516055-b083-487d-ade4-e7b301562bb7,
abstract = {{Platelet activation and aggregation has 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 viable bacteria escaped from the aggregates over time. This was not due to a differential activation in response to the bacteria as compared with physiological activators. All the bacteria isolates induced significant platelet activation, including integrin activation, alpha and dense granule release, at equivalent levels to potent physiological platelet activators that induced stable aggregates. The ability to escape the aggregates and resist antibacterial effects of platelets was dependent on active protein synthesis by the bacteria within the aggregate. We conclude that S. pyogenes can temporarily cover themselves with activated platelets and we propose that this may facilitate survival of bacteria in the presence of platelets.}},
author = {{Svensson, Lisbeth and Baumgarten, Maria and Mörgelin, Matthias and Shannon, Oonagh}},
issn = {{1098-5522}},
language = {{eng}},
number = {{10}},
pages = {{4307--4314}},
publisher = {{American Society for Microbiology}},
series = {{Infection and Immunity}},
title = {{Platelet activation by Streptococcus pyogenes leads to entrapment in platelet aggregates from which bacteria subsequently escape.}},
url = {{http://dx.doi.org/10.1128/IAI.02020-14}},
doi = {{10.1128/IAI.02020-14}},
volume = {{82}},
year = {{2014}},
}