Quantitative Analysis of Biofilm Formed on Vascular Prostheses by Staphylococcus Epidermidis with Different ica and aap Genetic Status

2013 ◽  
Vol 36 (2) ◽  
pp. 105-112 ◽  
Author(s):  
Joanna Golus ◽  
Magdalena Stankevic ◽  
Rafal Sawicki ◽  
Renata Los ◽  
Anna Malm ◽  
...  

Objectives This study aims to examine biofilm formed on vascular prostheses by Staphylococcus epidermidis with different ica and aap genetic status, and to evaluate the effect of antibiotic-modified prostheses on bacterial colonization. Methods Biofilm formation was determined using fluorescence microscopy imaging. Quantitative analysis was conducted using the biofilm coverage ratio (BCR) calculations. Results Our investigations prove that the BCR method with fluorescent dye enabled an accurate assessment of biofilm coverage and comparison of the obtained results. The ica+ aap+ strains formed a biofilm on all of the examined vascular prostheses. Uni-Graft® modified with covalently immobilized amikacin was effective in preventing bacterial adherence. Conclusions Molecular biology techniques combined with phenotype studies give a broad insight into biofilm formation mechanisms. On the other hand, fluorescence microscopy imaging along with BCR calculations are reliable and simple tools to quantitatively estimate biofilm formation, as well as the effectiveness of antimicrobial prosthesis modification.

2013 ◽  
Vol 24 (11) ◽  
pp. 1725-1734 ◽  
Author(s):  
Amanda L. Soohoo ◽  
Manojkumar A. Puthenveedu

Clathrin-mediated endocytosis has long been viewed as a process driven by core endocytic proteins, with internalized cargo proteins being passive. In contrast, an emerging view suggests that signaling receptor cargo may actively control its fate by regulating the dynamics of clathrin-coated pits (CCPs) that mediate their internalization. Despite its physiological implications, very little is known about such “cargo-mediated regulation” of CCPs by signaling receptors. Here, using multicolor total internal reflection fluorescence microscopy imaging and quantitative analysis in live cells, we show that the μ-opioid receptor, a physiologically relevant G protein–coupled signaling receptor, delays the dynamics of CCPs in which it is localized. This delay is mediated by the interactions of two critical leucines on the receptor cytoplasmic tail. Unlike the previously known mechanism of cargo-mediated regulation, these residues regulate the lifetimes of dynamin, a key component of CCP scission. These results identify a novel means for selectively controlling the endocytosis of distinct cargo that share common trafficking components and indicate that CCP regulation by signaling receptors can operate via divergent modes.


Author(s):  
Fernando Oliveira ◽  
Holger Rohde ◽  
Manuel Vilanova ◽  
Nuno Cerca

Staphylococcus epidermidis is one of the most important commensal microorganisms of human skin and mucosae. However, this bacterial species is also the cause of severe infections in immunocompromised patients, specially associated with the utilization of indwelling medical devices, that often serve as a scaffold for biofilm formation. S. epidermidis strains are often multidrug resistant and its association with biofilm formation makes these infections hard to treat. Their remarkable ability to form biofilms is widely regarded as its major pathogenic determinant. Although a significant amount of knowledge on its biofilm formation mechanisms has been achieved, we still do not understand how the species survives when exposed to the host harsh environment during invasion. A previous RNA-seq study highlighted that iron-metabolism associated genes were the most up-regulated bacterial genes upon contact with human blood, which suggested that iron acquisition plays an important role in S. epidermidis biofilm development and escape from the host innate immune system. In this perspective article, we review the available literature on the role of iron metabolism on S. epidermidis pathogenesis and propose that exploiting its dependence on iron could be pursued as a viable therapeutic alternative.


Open Medicine ◽  
2019 ◽  
Vol 15 (1) ◽  
pp. 14-21 ◽  
Author(s):  
Franca Vergalito ◽  
Laura Pietrangelo ◽  
Giulio Petronio Petronio ◽  
Federica Colitto ◽  
Marco Alfio Cutuli ◽  
...  

AbstractThe healthcare-associated infections (HCAIs) occur in patients both in nosocomial environments and in community. More often HCAIs are associated to the use of medical devices and bacterial biofilm development on these equipments. Due to the clinical and economic relevance of this topic, new strategies for the treatment of infections caused by biofilm proliferation are unceasingly searched by scientists.The present study investigated the role of vitamin E to reduce the biofilm formation for a larger panel of human pathogens, including strains of Staphylococcus aureus, Staphylococcus epidermidis, Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Acinetobacter baumannii, Pseudomonas aeruginosa and Pseudomonas putida.This potential activity was tested by placing a preparation of vitamin E (α-Tocopheryl acetate) as interface between the bacterial culture and the polystyrene walls of a 96 well plate at different concentrations of glucose, used as a biofilm enhancer.The Staphylococcus genus was further investigated by spreading the vitamin E on a silicone catheter lumen and evaluating its influence on the bacterial colonization.From our results, vitamin E has been able to interfere with bacterial biofilm and prevent in vitro biofilm formation. Furthermore, the ability of Staphylococcus aureus and Staphylococcus epidermidis to colonize the catheter surface decreased as a result of vitamin E application.


2012 ◽  
Vol 79 (4) ◽  
pp. 1393-1395 ◽  
Author(s):  
Llinos G. Harris ◽  
Yamni Nigam ◽  
James Sawyer ◽  
Dietrich Mack ◽  
David I. Pritchard

ABSTRACTStaphylococcus aureusandStaphylococcus epidermidisbiofilms cause chronic infections due to their ability to form biofilms. The excretions/secretions ofLucilia sericatalarvae (maggots) have effective activity for debridement and disruption of bacterial biofilms. In this paper, we demonstrate how chymotrypsin derived from maggot excretions/secretions disrupts protein-dependent bacterial biofilm formation mechanisms.


2005 ◽  
Vol 12 (1) ◽  
pp. 93-100 ◽  
Author(s):  
Daqian Sun ◽  
M. A. Accavitti ◽  
J. D. Bryers

ABSTRACT Staphylococcus epidermidis expresses a 140-kDa cell wall-bound protein accumulation-associated protein (AAP) to adhere to and accumulate as a biofilm on a surface. Potentially blocking AAP with a monoclonal antibody (MAb) could reduce or eliminate S. epidermidis bacterial colonization of biomedical devices. Here, we report on our efforts to (i) isolate AAP, (ii) generate MAbs against AAP, and (iii) determine the efficacy of MAbs to inhibit S. epidermidis biofilm formation. An M7 S. epidermidis mutant, reportedly deficient in AAP expression, was used as a negative control. Postinoculation murine sera, containing polyclonal antibodies against AAP, were able to reduce S. epidermidis biofilm formation by 54%. Select MAbs against AAP were able to reduce S. epidermidis by no more than 66%. Two MAb mixtures, 12C6/12A1 and 3C1/12A1, reduced S. epidermidis accumulation up to 79 and 87%, respectively, significantly more than individual MAbs. Contrary to a previous report, biofilm-deficient S. epidermidis mutant M7 expressed a 200-kDa protein on its cell wall that specifically bound AAP MAbs. Peptide characterization of this M7 protein by microcapillary reversed-phase high-pressure liquid chromatography-nanoelectrospray tandem mass spectrometry resulted in 53% homology with AAP. Ongoing studies will elucidate the dynamic expression of AAP and the M7 200-kDa protein in order to define their roles in biofilm formation.


2021 ◽  
Vol 10 (8) ◽  
pp. 1641
Author(s):  
Stefanie Kligman ◽  
Zhi Ren ◽  
Chun-Hsi Chung ◽  
Michael Angelo Perillo ◽  
Yu-Cheng Chang ◽  
...  

Implant surface design has evolved to meet oral rehabilitation challenges in both healthy and compromised bone. For example, to conquer the most common dental implant-related complications, peri-implantitis, and subsequent implant loss, implant surfaces have been modified to introduce desired properties to a dental implant and thus increase the implant success rate and expand their indications. Until now, a diversity of implant surface modifications, including different physical, chemical, and biological techniques, have been applied to a broad range of materials, such as titanium, zirconia, and polyether ether ketone, to achieve these goals. Ideal modifications enhance the interaction between the implant’s surface and its surrounding bone which will facilitate osseointegration while minimizing the bacterial colonization to reduce the risk of biofilm formation. This review article aims to comprehensively discuss currently available implant surface modifications commonly used in implantology in terms of their impact on osseointegration and biofilm formation, which is critical for clinicians to choose the most suitable materials to improve the success and survival of implantation.


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