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SufA – a bacterial enzyme that cleaves fibrinogen and blocks fibrin network formation
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 di...
Autores principales: | , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Microbiology Society
2009
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2885652/ https://www.ncbi.nlm.nih.gov/pubmed/19118364 http://dx.doi.org/10.1099/mic.0.021311-0 |
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author | Karlsson, Christofer Mörgelin, Matthias Collin, Mattias Lood, Rolf Andersson, Marie-Louise Schmidtchen, Artur Björck, Lars Frick, Inga-Maria |
author_facet | Karlsson, Christofer Mörgelin, Matthias Collin, Mattias Lood, Rolf Andersson, Marie-Louise Schmidtchen, Artur Björck, Lars Frick, Inga-Maria |
author_sort | Karlsson, Christofer |
collection | PubMed |
description | 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. |
format | Text |
id | pubmed-2885652 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | Microbiology Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-28856522010-07-06 SufA – a bacterial enzyme that cleaves fibrinogen and blocks fibrin network formation Karlsson, Christofer Mörgelin, Matthias Collin, Mattias Lood, Rolf Andersson, Marie-Louise Schmidtchen, Artur Björck, Lars Frick, Inga-Maria Microbiology (Reading) Microbial Pathogenicity 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. Microbiology Society 2009-01 /pmc/articles/PMC2885652/ /pubmed/19118364 http://dx.doi.org/10.1099/mic.0.021311-0 Text en Copyright © 2009, SGM http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Microbial Pathogenicity Karlsson, Christofer Mörgelin, Matthias Collin, Mattias Lood, Rolf Andersson, Marie-Louise Schmidtchen, Artur Björck, Lars Frick, Inga-Maria SufA – a bacterial enzyme that cleaves fibrinogen and blocks fibrin network formation |
title | SufA – a bacterial enzyme that cleaves fibrinogen and blocks fibrin network formation |
title_full | SufA – a bacterial enzyme that cleaves fibrinogen and blocks fibrin network formation |
title_fullStr | SufA – a bacterial enzyme that cleaves fibrinogen and blocks fibrin network formation |
title_full_unstemmed | SufA – a bacterial enzyme that cleaves fibrinogen and blocks fibrin network formation |
title_short | SufA – a bacterial enzyme that cleaves fibrinogen and blocks fibrin network formation |
title_sort | sufa – a bacterial enzyme that cleaves fibrinogen and blocks fibrin network formation |
topic | Microbial Pathogenicity |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2885652/ https://www.ncbi.nlm.nih.gov/pubmed/19118364 http://dx.doi.org/10.1099/mic.0.021311-0 |
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