scholarly journals Extracellular DNA release from the genome-reduced pathogen Mycoplasma hyopneumoniae is essential for biofilm formation on abiotic surfaces

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Benjamin B. A. Raymond ◽  
Cheryl Jenkins ◽  
Lynne Turnbull ◽  
Cynthia B. Whitchurch ◽  
Steven P. Djordjevic
Keyword(s):  
Biofilm Formation ◽  
Mycoplasma Hyopneumoniae ◽  
Extracellular Dna ◽  
Abiotic Surfaces ◽  
Dna Release

scholarly journals Biofilm Formation by Streptococcus pneumoniae: Role of Choline, Extracellular DNA, and Capsular Polysaccharide in Microbial Accretion

2006 ◽  
Vol 188 (22) ◽  
pp. 7785-7795 ◽  
Author(s):  
Miriam Moscoso ◽  
Ernesto García ◽  
Rubens López
Keyword(s):  
Streptococcus Pneumoniae ◽  
Biofilm Formation ◽  
Laser Scanning Microscopy ◽  
Extracellular Dna ◽  
Dimensional Structure ◽  
Confocal Laser ◽  
Upper Respiratory Tract ◽  
Teichoic Acids ◽  
Abiotic Surfaces ◽  
Biofilm Development

ABSTRACTStreptococcus pneumoniaecolonizes the human upper respiratory tract, and this asymptomatic colonization is known to precede pneumococcal disease. In this report, chemically defined and semisynthetic media were used to identify the initial steps of biofilm formation by pneumococcus during growth on abiotic surfaces such as polystyrene or glass. Unencapsulated pneumococci adhered to abiotic surfaces and formed a three-dimensional structure about 25 μm deep, as observed by confocal laser scanning microscopy and low-temperature scanning electron microscopy. Choline residues of cell wall teichoic acids were found to play a fundamental role in pneumococcal biofilm development. The role in biofilm formation of choline-binding proteins, which anchor to the teichoic acids of the cell envelope, was determined using unambiguously characterized mutants. The results showed that LytA amidase, LytC lysozyme, LytB glucosaminidase, CbpA adhesin, PcpA putative adhesin, and PspA (pneumococcal surface protein A) mutants had a decreased capacity to form biofilms, whereas no such reduction was observed in Pce phosphocholinesterase or CbpD putative amidase mutants. Moreover, encapsulated, clinical pneumococcal isolates were impaired in their capacity to form biofilms. In addition, a role for extracellular DNA and proteins in the establishment ofS. pneumoniaebiofilms was demonstrated. Taken together, these observations provide information on conditions that favor the sessile mode of growth byS. pneumoniae. The experimental approach described here should facilitate the study of bacterial genes that are required for biofilm formation. Those results, in turn, may provide insight into strategies to prevent pneumococcal colonization of its human host.

scholarly journals Low Levels of β-Lactam Antibiotics Induce Extracellular DNA Release and Biofilm Formation in Staphylococcus aureus

mBio ◽  
2012 ◽  
Vol 3 (4) ◽  
Author(s):  
Jeffrey B. Kaplan ◽  
Era A. Izano ◽  
Prerna Gopal ◽  
Michael T. Karwacki ◽  
Sangho Kim ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Biofilm Formation ◽  
Bacterial Biofilm ◽  
Extracellular Dna ◽  
Human Pathogen ◽  
Methicillin Resistant ◽  
Content Type ◽  
Low Level ◽  
Dna Release ◽  
Low Levels

ABSTRACTSubminimal inhibitory concentrations of antibiotics have been shown to induce bacterial biofilm formation. Few studies have investigated antibiotic-induced biofilm formation inStaphylococcus aureus, an important human pathogen. Our goal was to measureS. aureusbiofilm formation in the presence of low levels of β-lactam antibiotics. Fifteen phylogenetically diverse methicillin-resistantStaphylococcus aureus(MRSA) and methicillin-sensitiveS. aureus(MSSA) strains were employed. Methicillin, ampicillin, amoxicillin, and cloxacillin were added to cultures at concentrations ranging from 0× to 1× MIC. Biofilm formation was measured in 96-well microtiter plates using a crystal violet binding assay. Autoaggregation was measured using a visual test tube settling assay. Extracellular DNA was quantitated using agarose gel electrophoresis. All four antibiotics induced biofilm formation in some strains. The amount of biofilm induction was as high as 10-fold and was inversely proportional to the amount of biofilm produced by the strain in the absence of antibiotics. MRSA strains of lineages USA300, USA400, and USA500 exhibited the highest levels of methicillin-induced biofilm induction. Biofilm formation induced by low-level methicillin was inhibited by DNase. Low-level methicillin also induced DNase-sensitive autoaggregation and extracellular DNA release. The biofilm induction phenotype was absent in a strain deficient in autolysin (atl). Our findings demonstrate that subminimal inhibitory concentrations of β-lactam antibiotics significantly induce autolysin-dependent extracellular DNA release and biofilm formation in some strains ofS. aureus.IMPORTANCEThe widespread use of antibiotics as growth promoters in agriculture may expose bacteria to low levels of the drugs. The aim of this study was to investigate the effects of low levels of antibiotics on bacterial autoaggregation and biofilm formation, two processes that have been shown to foster genetic exchange and antibiotic resistance. We found that low levels of β-lactam antibiotics, a class commonly used in both clinical and agricultural settings, caused significant autoaggregation and biofilm formation by the important human pathogenStaphylococcus aureus. Both processes were dependent on cell lysis and release of DNA into the environment. The effect was most pronounced among multidrug-resistant strains known as methicillin-resistantS. aureus(MRSA). These results may shed light on the recalcitrance of some bacterial infections to antibiotic treatment in clinical settings and the evolution of antibiotic-resistant bacteria in agricultural settings.

scholarly journals Important Contribution of the Novel LocuscomEBto Extracellular DNA-Dependent Staphylococcus lugdunensis Biofilm Formation

2015 ◽  
Vol 83 (12) ◽  
pp. 4682-4692 ◽  
Author(s):  
Nithya Babu Rajendran ◽  
Julian Eikmeier ◽  
Karsten Becker ◽  
Muzaffar Hussain ◽  
Georg Peters ◽  
...  
Keyword(s):  
Biofilm Formation ◽  
Bacterial Species ◽  
Laser Scanning Microscopy ◽  
Extracellular Dna ◽  
Staphylococcus Lugdunensis ◽  
Content Type ◽  
Competence Gene ◽  
Independent Mechanism ◽  
Dna Release ◽  
The Impact

The coagulase-negative speciesStaphylococcus lugdunensisis an emerging cause of serious and potentially life-threatening infections, such as infective endocarditis. The pathogenesis of these infections is characterized by the ability ofS. lugdunensisto form biofilms on either biotic or abiotic surfaces. To elucidate the genetic basis of biofilm formation inS. lugdunensis, we performed transposon (Tn917) mutagenesis. One mutant had a significantly reduced biofilm-forming capacity and carried a Tn917insertion within the competence genecomEB. Site-directed mutagenesis and subsequent complementation with a functional copy ofcomEBverified the importance ofcomEBin biofilm formation. In several bacterial species, natural competence stimulates DNA release via lysis-dependent or -independent mechanisms. Extracellular DNA (eDNA) has been demonstrated to be an important structural component of many bacterial biofilms. Therefore, we quantified the eDNA in the biofilms and found diminished eDNA amounts in thecomEBmutant biofilm. High-resolution images and three-dimensional data obtained via confocal laser scanning microscopy (CSLM) visualized the impact of thecomEBmutation on biofilm integrity. ThecomEBmutant did not show reduced expression of autolysin genes, decreased autolytic activities, or increased cell viability, suggesting a cell lysis-independent mechanism of DNA release. Furthermore, reduced amounts of eDNA in thecomEBmutant biofilms did not result from elevated levels or activity of theS. lugdunensisthermonuclease NucI. In conclusion, we defined here, for the first time, a role for the competence genecomEBin staphylococcal biofilm formation. Our findings indicate thatcomEBstimulates biofilm formation via a lysis-independent mechanism of DNA release.

scholarly journals Effect of nicotine on Staphylococcus aureus biofilm formation and virulence factors

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Le Shi ◽  
Yang Wu ◽  
Chen Yang ◽  
Yue Ma ◽  
Qing-zhao Zhang ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Virulence Factors ◽  
Biofilm Formation ◽  
Alveolar Epithelial Cells ◽  
Extracellular Dna ◽  
Bacterial Invasion ◽  
Initial Attachment ◽  
Accessory Gene ◽  
Nicotine Treatment ◽  
Dna Release

AbstractStaphylococcus aureus is a common pathogen in chronic rhinosinusitis (CRS) patients, the pathogenesis of which involves the ability to form biofilms and produce various virulence factors. Tobacco smoke, another risk factor of CRS, facilitates S. aureus biofilm formation; however, the mechanisms involved are unclear. Here, we studied the effect of nicotine on S. aureus biofilm formation and the expression of virulence-related genes. S. aureus strains isolated from CRS patients and a USA300 strain were treated with nicotine or were untreated (control). Nicotine-treated S. aureus strains showed dose-dependent increases in biofilm formation, lower virulence, enhanced initial attachment, increased extracellular DNA release, and a higher autolysis rate, involving dysregulation of the accessory gene regulator (Agr) quorum-sensing system. Consequently, the expression of autolysis-related genes lytN and atlA, and the percentage of dead cells in biofilms was increased. However, the expression of virulence-related genes, including hla, hlb, pvl, nuc, ssp, spa, sigB, coa, and crtN was downregulated and there was reduced bacterial invasion of A549 human alveolar epithelial cells. The results of this study indicate that nicotine treatment enhances S. aureus biofilm formation by promoting initial attachment and extracellular DNA release but inhibits the virulence of this bacterium.

scholarly journals Extracellular DNA release confers heterogeneity in Candida albicans biofilm formation

2014 ◽  
Vol 14 (1) ◽  
Author(s):  
Ranjith Rajendran ◽  
Leighann Sherry ◽  
David F Lappin ◽  
Chris J Nile ◽  
Karen Smith ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Biofilm Formation ◽  
Extracellular Dna ◽  
Dna Release

scholarly journals PspC domain-containing protein (PCP) determines Streptococcus mutans biofilm formation through bacterial extracellular DNA release and platelet adhesion in experimental endocarditis

2021 ◽  
Vol 17 (2) ◽  
pp. e1009289
Author(s):  
Chiau-Jing Jung ◽  
Chih-Chieh Hsu ◽  
Jeng-Wei Chen ◽  
Hung-Wei Cheng ◽  
Chang-Tsu Yuan ◽  
...  
Keyword(s):  
Streptococcus Mutans ◽  
Biofilm Formation ◽  
Heart Valves ◽  
Platelet Adhesion ◽  
Bacterial Biofilm ◽  
Extracellular Dna ◽  
Dependent Manner ◽  
Dna Release

Bacterial extracellular DNA (eDNA) and activated platelets have been found to contribute to biofilm formation by Streptococcus mutans on injured heart valves to induce infective endocarditis (IE), yet the bacterial component directly responsible for biofilm formation or platelet adhesion remains unclear. Using in vivo survival assays coupled with microarray analysis, the present study identified a LiaR-regulated PspC domain-containing protein (PCP) in S. mutans that mediates bacterial biofilm formation in vivo. Reverse transcriptase- and chromatin immunoprecipitation-polymerase chain reaction assays confirmed the regulation of pcp by LiaR, while PCP is well-preserved among streptococcal pathogens. Deficiency of pcp reduced in vitro and in vivo biofilm formation and released the eDNA inside bacteria floe along with reduced bacterial platelet adhesion capacity in a fibrinogen-dependent manner. Therefore, LiaR-regulated PCP alone could determine release of bacterial eDNA and binding to platelets, thus contributing to biofilm formation in S. mutans-induced IE.

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