SufA - a bacterial enzyme that cleaves fibrinogen and blocks fibrin network formation.
Karlsson, Christofer LU ; Mörgelin, Matthias LU ; Collin, Mattias LU
; Lood, Rolf
LU
; Andersson, Marie-Louise
LU
; Schmidtchen, Artur
LU
; Björck, Lars
LU
and Frick, Inga-Maria
LU
(2009)
In Microbiology
155(Pt 1).
p.238-248
- Abstract
- Finegoldia magna is a member of the normal human bacterial flora on the skin and other non-sterile body surfaces, but this anaerobic coccus is also an important opportunistic pathogen. SufA was the first F. magna proteinase to be isolated and characterized. Many bacterial pathogens interfere with different steps of blood coagulation, and here we describe how purified SufA efficiently and specifically cleaves fibrinogen in human plasma. SufA is both secreted by F. magna and associated with the bacterial surface. Successful gene targeting has previously not been performed in anaerobic cocci, but in order to study the role of the SufA that is present at the bacterial surface, we constructed an F. magna mutant that expresses a truncated SufA... (More)
- Finegoldia magna is a member of the normal human bacterial flora on the skin and other non-sterile body surfaces, but this anaerobic coccus is also an important opportunistic pathogen. SufA was the first F. magna proteinase to be isolated and characterized. Many bacterial pathogens interfere with different steps of blood coagulation, and here we describe how purified SufA efficiently and specifically cleaves fibrinogen in human plasma. SufA is both secreted by F. magna and associated with the bacterial surface. Successful gene targeting has previously not been performed in anaerobic cocci, but in order to study the role of the SufA that is present at the bacterial surface, we constructed an F. magna mutant that expresses a truncated SufA lacking proteolytic activity. In contrast to wild-type bacteria that delayed the coagulation of human plasma, mutant bacteria had no such effect. Wild-type and mutant bacteria adhered to keratinocytes equally well, but in a plasma environment only wild-type bacteria blocked the formation of fibrin networks surrounding adherent bacteria. The effective cleavage of fibrinogen by SufA suggests that the interference with fibrin network formation represents an adaptive mechanism of F. magna with potential implications also for pathogenicity. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1290037
- author
- Karlsson, Christofer
LU
; Mörgelin, Matthias
LU
; Collin, Mattias
LU
; Lood, Rolf
LU
; Andersson, Marie-Louise
LU
; Schmidtchen, Artur
LU
; Björck, Lars
LU
and Frick, Inga-Maria
LU
- organization
- publishing date
- 2009
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Microbiology
- volume
- 155
- issue
- Pt 1
- pages
- 238 - 248
- publisher
- MAIK Nauka/Interperiodica
- external identifiers
-
- wos:000262730400025
- pmid:19118364
- scopus:61449101478
- pmid:19118364
- ISSN
- 1465-2080
- DOI
- 10.1099/mic.0.021311-0
- language
- English
- LU publication?
- yes
- id
- 64b25982-b2bb-4a96-9ce3-f4e343489bdd (old id 1290037)
- alternative location
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2885652/
- date added to LUP
- 2016-04-04 07:07:35
- date last changed
- 2022-01-29 01:44:11
@article{64b25982-b2bb-4a96-9ce3-f4e343489bdd,
abstract = {{Finegoldia magna is a member of the normal human bacterial flora on the skin and other non-sterile body surfaces, but this anaerobic coccus is also an important opportunistic pathogen. SufA was the first F. magna proteinase to be isolated and characterized. Many bacterial pathogens interfere with different steps of blood coagulation, and here we describe how purified SufA efficiently and specifically cleaves fibrinogen in human plasma. SufA is both secreted by F. magna and associated with the bacterial surface. Successful gene targeting has previously not been performed in anaerobic cocci, but in order to study the role of the SufA that is present at the bacterial surface, we constructed an F. magna mutant that expresses a truncated SufA lacking proteolytic activity. In contrast to wild-type bacteria that delayed the coagulation of human plasma, mutant bacteria had no such effect. Wild-type and mutant bacteria adhered to keratinocytes equally well, but in a plasma environment only wild-type bacteria blocked the formation of fibrin networks surrounding adherent bacteria. The effective cleavage of fibrinogen by SufA suggests that the interference with fibrin network formation represents an adaptive mechanism of F. magna with potential implications also for pathogenicity.}},
author = {{Karlsson, Christofer and Mörgelin, Matthias and Collin, Mattias and Lood, Rolf and Andersson, Marie-Louise and Schmidtchen, Artur and Björck, Lars and Frick, Inga-Maria}},
issn = {{1465-2080}},
language = {{eng}},
number = {{Pt 1}},
pages = {{238--248}},
publisher = {{MAIK Nauka/Interperiodica}},
series = {{Microbiology}},
title = {{SufA - a bacterial enzyme that cleaves fibrinogen and blocks fibrin network formation.}},
url = {{http://dx.doi.org/10.1099/mic.0.021311-0}},
doi = {{10.1099/mic.0.021311-0}},
volume = {{155}},
year = {{2009}},
}