scholarly journals Bacterial biofilms in infective endocarditis: an in vitro model to investigate emerging technologies of antimicrobial cardiovascular device coatings

2020 ◽  
Author(s):  
Alexander Lauten ◽  
Marc Martinović ◽  
Laura Kursawe ◽  
Judith Kikhney ◽  
Klaus Affeld ◽  
...  
Keyword(s):  
Infective Endocarditis ◽  
In Vitro Model ◽  
Emerging Technologies ◽  
Bacterial Biofilms ◽  
Vitro Model

Bacterial Biofilms in Infective Endocarditis – A complex in vitro - Model to Investigate Emerging Technologies of Antimicrobial Cardiovascular Device Coatings

2020 ◽  
Author(s):  
Laura Kursawe ◽  
Alexander Lauten ◽  
Marc Martinović ◽  
Klaus Affeld ◽  
Ulrich Kertzscher ◽  
...  
Keyword(s):  
Infective Endocarditis ◽  
Heart Valves ◽  
In Vitro Model ◽  
Bacterial Biofilm ◽  
Bacterial Biofilms ◽  
Aortic Valves ◽  
Biofilm Growth ◽  
Vitro Model ◽  
Biofilm Development

<p><strong>Objective:</strong> Most biofilm flow-chambers are designed for standardized homogeneous biofilms for research purposes. These do not mimic the complexity of prosthetic heart valves, which consist of both artificial and biological material.</p> <p>Infective endocarditis (IE) is still associated with a high morbidity and mortality. IE is characterized by bacterial biofilms of the endocardium leading to destruction of the valve. Current research demonstrates that about one quarter of the patients with formal surgery indication cannot undergo surgery. This group of patients needs further options of therapy, but due to a lack of models for IE, prospects of research are low.</p> <p>Therefore, the purpose of this project was to establish an in vitro - model of infective endocarditis to allow growth of bacterial biofilms on porcine aortic valves, serving as baseline for further research.</p> <p><strong>Methods and Results: </strong>A pulsatile two-chamber circulation model was constructed that kept native porcine aortic valves under sterile, physiologic hemodynamic and temperature conditions. To exclude external contamination, sterility tests with sterile culture media were performed for 24h. During this time period, no growth of microorganisms was observed in the system and cultures after plating on standard media remained negative.</p> <p>The system was inoculated with Staphylococcus epidermidis PIA 8400 to create biofilms on porcine aortic valves. Porcine aortic roots were incubated in this system for increasing periods of time and bacterial titration to evaluate bacterial growth and biofilm development on the valves. After incubation, specimens were embedded and tissue sections were analyzed by Fluorescence in situ hybridization (FISH) for direct visualization of the biofilms and bacterial activity.</p> <p>Pilot tests for biofilm growth showed monospecies colonization consisting of cocci with time- and inocula-dependent increase. FISH visualized biofilms with ribosome-containing, and thus metabolic active cocci, tissue infiltration and similar colonization pattern as observed by FISH in human IE heart valves infected by S. epidermidis.</p> <p><strong>Conclusion:</strong> These results demonstrate the establishment of a novel complex in vitro - model for bacterial biofilm growth on porcine aortic roots. The model will allow identifying predilection sites of heart valves for bacterial adhesion and biofilm growth and it may serve as baseline for further research on IE therapy and prevention, e.g. the development of antimicrobial transcatheter approaches to IE.</p>

Stem cells in neurotoxicology: Human in vitro model combined with emerging technologies

2008 ◽  
Vol 180 ◽  
pp. S8
Author(s):  
Leonora Buzanska ◽  
Ana Ruiz ◽  
Laura Ceriotti ◽  
Tomasz Sobanski ◽  
Helena Hogberg ◽  
...  
Keyword(s):  
Stem Cells ◽  
In Vitro Model ◽  
Emerging Technologies ◽  
Vitro Model

scholarly journals CRT-700.58 A Pulsatile In Vitro-model of Infective Endocarditis

2018 ◽  
Vol 11 (4) ◽  
pp. S65
Author(s):  
Marc Martinovic ◽  
Hans R. Figulla ◽  
Alexander Lauten
Keyword(s):  
Infective Endocarditis ◽  
In Vitro Model ◽  
Vitro Model

A dynamic in vitro model for evaluating antimicrobial activity against bacterial biofilms using a new device and clinical-used catheters

2010 ◽  
Vol 83 (3) ◽  
pp. 307-311 ◽  
Author(s):  
Isabel García ◽  
Ma del Carmen Conejo ◽  
Antonio Ojeda ◽  
Jesús Rodríguez-Baño ◽  
Alvaro Pascual
Keyword(s):  
Antimicrobial Activity ◽  
In Vitro Model ◽  
Bacterial Biofilms ◽  
New Device ◽  
Vitro Model

Bacterial tissue tropism: an in vitro model for infective endocarditis

1987 ◽  
Vol 21 (11) ◽  
pp. 813-820 ◽  
Author(s):  
R. C BECKER ◽  
P. M DiBELLO ◽  
F. V LUCAS
Keyword(s):  
Infective Endocarditis ◽  
In Vitro Model ◽  
Tissue Tropism ◽  
Vitro Model

scholarly journals Influence of Platelets and Platelet Microbicidal Protein Susceptibility on the Fate of Staphylococcus aureusin an In Vitro Model of Infective Endocarditis

2000 ◽  
Vol 68 (8) ◽  
pp. 4699-4705 ◽  
Author(s):  
Renee-Claude Mercier ◽  
Michael J. Rybak ◽  
Arnold S. Bayer ◽  
Michael R. Yeaman
Keyword(s):  
Infective Endocarditis ◽  
Platelet Activation ◽  
Host Defense ◽  
In Vitro Model ◽  
In Vitro Susceptibility ◽  
Principal Mechanism ◽  
Platelet Microbicidal Protein ◽  
Vitro Model ◽  
Time Kill

ABSTRACT Several lines of evidence indicate that platelets protect against endovascular infections such as infective endocarditis (IE). It is highly likely that a principal mechanism of this platelet host defense role is the release of platelet microbicidal proteins (PMPs) in response to agonists generated at sites of endovascular infection. We studied the ability of platelets to limit the colonization and proliferation of Staphylococcus aureus in an in vitro model of IE. Three isogenic S. aureus strains, differing in their in vitro susceptibility to thrombin-induced platelet microbicidal protein-1 (tPMP), were used: ISP479C (parental strain; highly susceptible to tPMP [tPMPs]); ISP479R (transposon mutant derived from ISP479; tPMP resistant [tPMPr]); or 757-5 (tPMPr transductant of the ISP479R genotype in the ISP479 parental background). Time-kill assays and in vitro IE models were used to examine the temporal relationship between thrombin-induced platelet activation and S. aureus killing. In time-kill studies, early platelet activation (30 min prior to bacterial exposure) correlated with a significant bactericidal effect against tPMPs ISP479C (r 2 > 0.90,P < 0.02) but not against tPMPr strains, ISP479R or 757-5. In the IE model, thrombin activation significantly inhibited proliferation of ISP479C within simulated vegetations compared to strains ISP479R or 757-5 (P < 0.05). The latter differences were observed despite there being no detectable differences among the three S. aureus strains in initial colonization of simulated vegetations. Collectively, these data indicate that platelets limit intravegetation proliferation of tPMPs but not tPMPr S. aureus. These findings underscore the likelihood that platelets play an important antimicrobial host defense role in preventing and/or limiting endovascular infections due to tPMPs pathogens.

An in vitro model for investigation of vitamin A effects on wound healing

2021 ◽  
pp. 1-6
Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid
Keyword(s):  
Wound Healing ◽  
Endothelial Cell ◽  
Vitamin A ◽  
In Vitro Model ◽  
Cellular Proliferation ◽  
Endothelial Cell Migration ◽  
Normal Fibroblast ◽  
Anti Inflammatory ◽  
Vitro Model

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.

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