A novel in vitro model for hematogenous spreading of S. aureus device biofilms demonstrating clumping dispersal as an advantageous dissemination mechanism

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Resumé

Staphylococcus aureus is able to disseminate from vascular device biofilms to the blood and organs, resulting in life-threatening infections such as endocarditis. The mechanisms behind spreading are largely unknown, especially how the bacterium escapes immune effectors and antibiotics in the process. Using an in vitro catheter infection model, we studied S. aureus biofilm growth, late-stage dispersal, and reattachment to downstream endothelial cell layers. The ability of the released biofilm material to resist host response and disseminate in vivo was furthermore studied in whole blood- and phagocyte survival assays, and in a short-term murine infection model. We found that S. aureus biofilms formed in flow of human plasma release biofilm thromboemboli with embedded bacteria and bacteria-secreted polysaccharides. The emboli disseminate as antibiotic and immune resistant vehicles that hold the ability to adhere to and initiate colonization of endothelial cell layers under flow. In vivo experiments showed that the released biofilm material reached the heart similarly as ordinary broth-grown bacteria, but also that clumps to some extend were trapped in the lungs. The clumping dispersal of S. aureus from in vivo-like vascular biofilms and their specific properties demonstrated here help explain the pathophysiology associated with S. aureus bloodstream infections.
OriginalsprogEngelsk
Artikelnummere12785
TidsskriftCellular Microbiology
Vol/bind19
Udgave nummer12
Antal sider13
ISSN1462-5814
DOI
StatusUdgivet - 2017

Fingeraftryk

Biofilms
Equipment and Supplies
Phagocytes
In Vitro Techniques
Catheters
Lung
Growth

Citer dette

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title = "A novel in vitro model for hematogenous spreading of S. aureus device biofilms demonstrating clumping dispersal as an advantageous dissemination mechanism",
abstract = "Staphylococcus aureus is able to disseminate from vascular device biofilms to the blood and organs, resulting in life-threatening infections such as endocarditis. The mechanisms behind spreading are largely unknown, especially how the bacterium escapes immune effectors and antibiotics in the process. Using an in vitro catheter infection model, we studied S. aureus biofilm growth, late-stage dispersal, and reattachment to downstream endothelial cell layers. The ability of the released biofilm material to resist host response and disseminate in vivo was furthermore studied in whole blood- and phagocyte survival assays, and in a short-term murine infection model. We found that S. aureus biofilms formed in flow of human plasma release biofilm thromboemboli with embedded bacteria and bacteria-secreted polysaccharides. The emboli disseminate as antibiotic and immune resistant vehicles that hold the ability to adhere to and initiate colonization of endothelial cell layers under flow. In vivo experiments showed that the released biofilm material reached the heart similarly as ordinary broth-grown bacteria, but also that clumps to some extend were trapped in the lungs. The clumping dispersal of S. aureus from in vivo-like vascular biofilms and their specific properties demonstrated here help explain the pathophysiology associated with S. aureus bloodstream infections.",
author = "Gr{\o}nnemose, {Rasmus Birkholm} and {Lindhardt S{\ae}derup (Madsen)}, Kirstine and Kolmos, {Hans J{\o}rn} and S{\o}ren Hansen and {Antoinette Asferg}, Cecilie and Rasmussen, {Karina Juhl} and Yaseelan Palarasah and Andersen, {Thomas Emil}",
year = "2017",
doi = "10.1111/cmi.12785",
language = "English",
volume = "19",
journal = "Cellular Microbiology",
issn = "1462-5814",
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TY - JOUR

T1 - A novel in vitro model for hematogenous spreading of S. aureus device biofilms demonstrating clumping dispersal as an advantageous dissemination mechanism

AU - Grønnemose, Rasmus Birkholm

AU - Lindhardt Sæderup (Madsen), Kirstine

AU - Kolmos, Hans Jørn

AU - Hansen, Søren

AU - Antoinette Asferg, Cecilie

AU - Rasmussen, Karina Juhl

AU - Palarasah, Yaseelan

AU - Andersen, Thomas Emil

PY - 2017

Y1 - 2017

N2 - Staphylococcus aureus is able to disseminate from vascular device biofilms to the blood and organs, resulting in life-threatening infections such as endocarditis. The mechanisms behind spreading are largely unknown, especially how the bacterium escapes immune effectors and antibiotics in the process. Using an in vitro catheter infection model, we studied S. aureus biofilm growth, late-stage dispersal, and reattachment to downstream endothelial cell layers. The ability of the released biofilm material to resist host response and disseminate in vivo was furthermore studied in whole blood- and phagocyte survival assays, and in a short-term murine infection model. We found that S. aureus biofilms formed in flow of human plasma release biofilm thromboemboli with embedded bacteria and bacteria-secreted polysaccharides. The emboli disseminate as antibiotic and immune resistant vehicles that hold the ability to adhere to and initiate colonization of endothelial cell layers under flow. In vivo experiments showed that the released biofilm material reached the heart similarly as ordinary broth-grown bacteria, but also that clumps to some extend were trapped in the lungs. The clumping dispersal of S. aureus from in vivo-like vascular biofilms and their specific properties demonstrated here help explain the pathophysiology associated with S. aureus bloodstream infections.

AB - Staphylococcus aureus is able to disseminate from vascular device biofilms to the blood and organs, resulting in life-threatening infections such as endocarditis. The mechanisms behind spreading are largely unknown, especially how the bacterium escapes immune effectors and antibiotics in the process. Using an in vitro catheter infection model, we studied S. aureus biofilm growth, late-stage dispersal, and reattachment to downstream endothelial cell layers. The ability of the released biofilm material to resist host response and disseminate in vivo was furthermore studied in whole blood- and phagocyte survival assays, and in a short-term murine infection model. We found that S. aureus biofilms formed in flow of human plasma release biofilm thromboemboli with embedded bacteria and bacteria-secreted polysaccharides. The emboli disseminate as antibiotic and immune resistant vehicles that hold the ability to adhere to and initiate colonization of endothelial cell layers under flow. In vivo experiments showed that the released biofilm material reached the heart similarly as ordinary broth-grown bacteria, but also that clumps to some extend were trapped in the lungs. The clumping dispersal of S. aureus from in vivo-like vascular biofilms and their specific properties demonstrated here help explain the pathophysiology associated with S. aureus bloodstream infections.

U2 - 10.1111/cmi.12785

DO - 10.1111/cmi.12785

M3 - Journal article

VL - 19

JO - Cellular Microbiology

JF - Cellular Microbiology

SN - 1462-5814

IS - 12

M1 - e12785

ER -