Staphylococcus aureus induced clotting of plasma is an immune evasion mechanism to persist within the fibrin network.
Loof, Torsten LU ; Goldmann, Oliver ; Naudin, Clément LU ; Mörgelin, Matthias LU ; Neumann, Yvonne ; Pils, Marina ; Foster, Simon ; Medina, Eva and Herwald, Heiko LU
(2014)
In Microbiology
- Abstract
- Recent work has shown that coagulation and innate immunity are tightly interwoven host responses that help eradicate an invading pathogen. Some bacterial species including Staphylococcus aureus secrete pro-coagulant factors that in turn can modulate these immune reactions. Such mechanisms may not only protect the microorganism from a lethal attack, but also promote bacterial proliferation and the establishment of the infection. Our data show that coagulase positive S. aureus bacteria promote clotting of plasma which was not seen when a coagulase-deficient mutant strain was used. Further in vitro studies show that this ability constitutes a mechanism that supports the aggregation, survival, and persistence of the microorganism within the... (More)
- Recent work has shown that coagulation and innate immunity are tightly interwoven host responses that help eradicate an invading pathogen. Some bacterial species including Staphylococcus aureus secrete pro-coagulant factors that in turn can modulate these immune reactions. Such mechanisms may not only protect the microorganism from a lethal attack, but also promote bacterial proliferation and the establishment of the infection. Our data show that coagulase positive S. aureus bacteria promote clotting of plasma which was not seen when a coagulase-deficient mutant strain was used. Further in vitro studies show that this ability constitutes a mechanism that supports the aggregation, survival, and persistence of the microorganism within the fibrin network. These findings were also confirmed when agglutination and persistence of coagulase-positive S. aureus bacteria at the local focus of infection were studied in a subcutaneous murine infection model. In contrast, the coagulase-deficient S. aureus strain which was not able to induce clotting failed to aggregate and to persist in vivo. In conclusion our data suggest that coagulase positive S. aureus have evolved mechanisms that prevent their elimination within a fibrin clot. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4905742
- author
- Loof, Torsten
LU
; Goldmann, Oliver
; Naudin, Clément
LU
; Mörgelin, Matthias
LU
; Neumann, Yvonne
; Pils, Marina
; Foster, Simon
; Medina, Eva
and Herwald, Heiko
LU
- organization
- publishing date
- 2014
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Microbiology
- publisher
- MAIK Nauka/Interperiodica
- external identifiers
-
- pmid:25533444
- pmid:25533444
- wos:000376048000014
- scopus:84923610968
- ISSN
- 1465-2080
- DOI
- 10.1099/mic.0.000019
- language
- English
- LU publication?
- yes
- id
- 003c0fa2-8695-43fb-95f8-155418464611 (old id 4905742)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/25533444?dopt=Abstract
- date added to LUP
- 2016-04-04 08:56:24
- date last changed
- 2022-03-23 03:30:38
@article{003c0fa2-8695-43fb-95f8-155418464611,
abstract = {{Recent work has shown that coagulation and innate immunity are tightly interwoven host responses that help eradicate an invading pathogen. Some bacterial species including Staphylococcus aureus secrete pro-coagulant factors that in turn can modulate these immune reactions. Such mechanisms may not only protect the microorganism from a lethal attack, but also promote bacterial proliferation and the establishment of the infection. Our data show that coagulase positive S. aureus bacteria promote clotting of plasma which was not seen when a coagulase-deficient mutant strain was used. Further in vitro studies show that this ability constitutes a mechanism that supports the aggregation, survival, and persistence of the microorganism within the fibrin network. These findings were also confirmed when agglutination and persistence of coagulase-positive S. aureus bacteria at the local focus of infection were studied in a subcutaneous murine infection model. In contrast, the coagulase-deficient S. aureus strain which was not able to induce clotting failed to aggregate and to persist in vivo. In conclusion our data suggest that coagulase positive S. aureus have evolved mechanisms that prevent their elimination within a fibrin clot.}},
author = {{Loof, Torsten and Goldmann, Oliver and Naudin, Clément and Mörgelin, Matthias and Neumann, Yvonne and Pils, Marina and Foster, Simon and Medina, Eva and Herwald, Heiko}},
issn = {{1465-2080}},
language = {{eng}},
publisher = {{MAIK Nauka/Interperiodica}},
series = {{Microbiology}},
title = {{Staphylococcus aureus induced clotting of plasma is an immune evasion mechanism to persist within the fibrin network.}},
url = {{http://dx.doi.org/10.1099/mic.0.000019}},
doi = {{10.1099/mic.0.000019}},
year = {{2014}},
}