scholarly journals Cigarette Smoke Increases Staphylococcus aureus Biofilm Formation via Oxidative Stress

2012 ◽  
Vol 80 (11) ◽  
pp. 3804-3811 ◽  
Author(s):  
Ritwij Kulkarni ◽  
Swati Antala ◽  
Alice Wang ◽  
Fábio E. Amaral ◽  
Ryan Rampersaud ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Cigarette Smoke ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Protein A ◽  
Model Organism ◽  
Human Cells ◽  
Dependent Manner ◽  
Content Type ◽  
Tract Infections

ABSTRACTThe strong epidemiological association between cigarette smoke (CS) exposure and respiratory tract infections is conventionally attributed to immunosuppressive and irritant effects of CS on human cells. Since pathogenic bacteria such asStaphylococcus aureusare members of the normal microbiota and reside in close proximity to human nasopharyngeal cells, we hypothesized that bioactive components of CS might affect these organisms and potentiate their virulence. UsingStaphylococcus aureusas a model organism, we observed that the presence of CS increased both biofilm formation and host cell adherence. Analysis of putative molecular pathways revealed that CS exposure decreased expression of the quorum-sensingagrsystem, which is involved in biofilm dispersal, and increased transcription of biofilm inducers such assarAandrbf. CS contains bioactive compounds, including free radicals and reactive oxygen species, and we observed transcriptional induction of bacterial oxidoreductases, including superoxide dismutase, following exposure. Moreover, pretreatment of CS with an antioxidant abrogated CS-mediated enhancement of biofilms. Exposure of bacteria to hydrogen peroxide alone increased biofilm formation. These observations are consistent with the hypothesis that CS induces staphylococcal biofilm formation in an oxidant-dependent manner. CS treatment induced transcription offnbA(encoding fibronectin binding protein A), leading to increased binding of CS-treated staphylococci to immobilized fibronectin and increased adherence to human cells. These observations indicate that the bioactive effects of CS may extend to the resident microbiota of the nasopharynx, with implications for the pathogenesis of respiratory infection in CS-exposed humans.

scholarly journals Protein A-Mediated Multicellular Behavior in Staphylococcus aureus

2008 ◽  
Vol 191 (3) ◽  
pp. 832-843 ◽  
Author(s):  
Nekane Merino ◽  
Alejandro Toledo-Arana ◽  
Marta Vergara-Irigaray ◽  
Jaione Valle ◽  
Cristina Solano ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Biofilm Formation ◽  
Protein A ◽  
Surface Proteins ◽  
Growth Media ◽  
Dependent Manner ◽  
Chronic Infections ◽  
The Matrix ◽  
Implanted Medical Devices ◽  
Biofilm Development

ABSTRACT The capacity of Staphylococcus aureus to form biofilms on host tissues and implanted medical devices is one of the major virulence traits underlying persistent and chronic infections. The matrix in which S. aureus cells are encased in a biofilm often consists of the polysaccharide intercellular adhesin (PIA) or poly-N-acetyl glucosamine (PNAG). However, surface proteins capable of promoting biofilm development in the absence of PIA/PNAG exopolysaccharide have been described. Here, we used two-dimensional nano-liquid chromatography and mass spectrometry to investigate the composition of a proteinaceous biofilm matrix and identified protein A (spa) as an essential component of the biofilm; protein A induced bacterial aggregation in liquid medium and biofilm formation under standing and flow conditions. Exogenous addition of synthetic protein A or supernatants containing secreted protein A to growth media induced biofilm development, indicating that protein A can promote biofilm development without being covalently anchored to the cell wall. Protein A-mediated biofilm formation was completely inhibited in a dose-dependent manner by addition of serum, purified immunoglobulin G, or anti-protein A-specific antibodies. A murine model of subcutaneous catheter infection unveiled a significant role for protein A in the development of biofilm-associated infections, as the amount of protein A-deficient bacteria recovered from the catheter was significantly lower than that of wild-type bacteria when both strains were used to coinfect the implanted medical device. Our results suggest a novel role for protein A complementary to its known capacity to interact with multiple immunologically important eukaryotic receptors.

scholarly journals HtrA Is Important for Stress Resistance and Virulence in Haemophilus parasuis

2016 ◽  
Vol 84 (8) ◽  
pp. 2209-2219 ◽  
Author(s):  
Luhua Zhang ◽  
Ying Li ◽  
Yiping Wen ◽  
Gee W. Lau ◽  
Xiaobo Huang ◽  
...  
Keyword(s):  
Biofilm Formation ◽  
Protein Quality ◽  
Protein A ◽  
Opportunistic Pathogen ◽  
Dependent Manner ◽  
Haemophilus Parasuis ◽  
Content Type ◽  
Outer Membrane Protein A ◽  
Dipeptide Transport ◽  
Atp Binding Protein

Haemophilus parasuisis an opportunistic pathogen that causes Glässer's disease in swine, with polyserositis, meningitis, and arthritis. The high-temperature requirement A (HtrA)-like protease, which is involved in protein quality control, has been reported to be a virulence factor in many pathogens. In this study, we showed that HtrA ofH. parasuis(HpHtrA) exhibited both chaperone and protease activities. Finally, nickel import ATP-binding protein (NikE), periplasmic dipeptide transport protein (DppA), and outer membrane protein A (OmpA) were identified as proteolytic substrates for HpHtrA. The protease activity reached its maximum at 40°C in a time-dependent manner. Disruption of thehtrAgene from strain SC1401 affected tolerance to temperature stress and resistance to complement-mediated killing. Furthermore, increased autoagglutination and biofilm formation were detected in thehtrAmutant. In addition, thehtrAmutant was significantly attenuated in virulence in the murine model of infection. Together, these data demonstrate that HpHtrA plays an important role in the virulence ofH. parasuis.

scholarly journals Staphylococcus aureus Fibronectin-Binding Protein A Mediates Cell-Cell Adhesion through Low-Affinity Homophilic Bonds

mBio ◽  
2015 ◽  
Vol 6 (3) ◽  
Author(s):  
Philippe Herman-Bausier ◽  
Sofiane El-Kirat-Chatel ◽  
Timothy J. Foster ◽  
Joan A. Geoghegan ◽  
Yves F. Dufrêne
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Surface ◽  
Biofilm Formation ◽  
Protein A ◽  
Intercellular Adhesion ◽  
Surface Proteins ◽  
Content Type ◽  
Fibronectin Binding ◽  
A Domains ◽  
Cell Cell

ABSTRACT Staphylococcus aureus is an important opportunistic pathogen which is a leading cause of biofilm-associated infections on indwelling medical devices. The cell surface-located fibronectin-binding protein A (FnBPA) plays an important role in the accumulation phase of biofilm formation by methicillin-resistant S. aureus (MRSA), but the underlying molecular interactions are not yet established. Here, we use single-cell and single-molecule atomic force microscopy to unravel the mechanism by which FnBPA mediates intercellular adhesion. We show that FnBPA is responsible for specific cell-cell interactions that involve the FnBPA A domain and cause microscale cell aggregation. We demonstrate that the strength of FnBPA-mediated adhesion originates from multiple low-affinity homophilic interactions between FnBPA A domains on neighboring cells. Low-affinity binding by means of FnBPA may be important for biofilm dynamics. These results provide a molecular basis for the ability of FnBPA to promote cell accumulation during S. aureus biofilm formation. We speculate that homophilic interactions may represent a generic strategy among staphylococcal cell surface proteins for guiding intercellular adhesion. As biofilm formation by MRSA strains depends on proteins rather than polysaccharides, our approach offers exciting prospects for the design of drugs or vaccines to inhibit protein-dependent intercellular interactions in MRSA biofilms. IMPORTANCE Staphylococcus aureus is a human pathogen that forms biofilms on indwelling medical devices, such as central venous catheters and prosthetic joints. This leads to biofilm infections that are difficult to treat with antibiotics because many cells within the biofilm matrix are dormant. The fibronectin-binding proteins (FnBPs) FnBPA and FnBPB promote biofilm formation by clinically relevant methicillin-resistant S. aureus (MRSA) strains, but the molecular mechanisms involved remain poorly understood. We used atomic force microscopy techniques to demonstrate that FnBPA mediates cell-cell adhesion via multiple, low-affinity homophilic bonds between FnBPA A domains on adjacent cells. Therefore, FnBP-mediated homophilic interactions represent an interesting target to prevent MRSA biofilms. We propose that such homophilic mechanisms may be widespread among staphylococcal cell surface proteins, providing a means to guide intercellular adhesion and biofilm accumulation.

scholarly journals Tannic Acid Inhibits Staphylococcus aureus Surface Colonization in an IsaA-Dependent Manner

2012 ◽  
Vol 81 (2) ◽  
pp. 496-504 ◽  
Author(s):  
David E. Payne ◽  
Nicholas R. Martin ◽  
Katherine R. Parzych ◽  
Alex H. Rickard ◽  
Adam Underwood ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Tannic Acid ◽  
Biofilm Formation ◽  
Antibiofilm Activity ◽  
Host Immune System ◽  
Dependent Manner ◽  
Content Type ◽  
Surface Colonization ◽  
Biofilm Development ◽  
Insight Into

ABSTRACTStaphylococcus aureusis a human commensal and pathogen that is capable of forming biofilms on a variety of host tissues and implanted medical devices. Biofilm-associated infections resist antimicrobial chemotherapy and attack from the host immune system, making these infections particularly difficult to treat. In order to gain insight into environmental conditions that influenceS. aureusbiofilm development, we screened a library of small molecules for the ability to inhibitS. aureusbiofilm formation. This led to the finding that the polyphenolic compound tannic acid inhibitsS. aureusbiofilm formation in multiple biofilm models without inhibiting bacterial growth. We present evidence that tannic acid inhibitsS. aureusbiofilm formation via a mechanism dependent upon the putative transglycosylase IsaA. Tannic acid did not inhibit biofilm formation of anisaAmutant. Overexpression of wild-type IsaA inhibited biofilm formation, whereas overexpression of a catalytically dead IsaA had no effect. Tannin-containing drinks like tea have been found to reduce methicillin-resistantS. aureusnasal colonization. We found that black tea inhibitedS. aureusbiofilm development and that anisaAmutant resisted this inhibition. Antibiofilm activity was eliminated from tea when milk was added to precipitate the tannic acid. Finally, we developed a rodent model forS. aureusthroat colonization and found that tea consumption reducedS. aureusthroat colonization via anisaA-dependent mechanism. These findings provide insight into a molecular mechanism by which commonly consumed polyphenolic compounds, such as tannins, influenceS. aureussurface colonization.

scholarly journals SaeRS Is Responsive to Cellular Respiratory Status and Regulates Fermentative Biofilm Formation in Staphylococcus aureus

2017 ◽  
Vol 85 (8) ◽  
Author(s):  
Ameya A. Mashruwala ◽  
Casey M. Gries ◽  
Tyler D. Scherr ◽  
Tammy Kielian ◽  
Jeffrey M. Boyd
Keyword(s):  
Staphylococcus Aureus ◽  
Biofilm Formation ◽  
Protein A ◽  
Regulatory System ◽  
Cellular Respiration ◽  
Signal Molecule ◽  
Terminal Electron Acceptor ◽  
Content Type ◽  
Respiratory Status

ABSTRACT Biofilms are multicellular communities of microorganisms living as a quorum rather than as individual cells. The bacterial human pathogen Staphylococcus aureus uses oxygen as a terminal electron acceptor during respiration. Infected human tissues are hypoxic or anoxic. We recently reported that impaired respiration elicits a programmed cell lysis (PCL) phenomenon in S. aureus leading to the release of cellular polymers that are utilized to form biofilms. PCL is dependent upon the AtlA murein hydrolase and is regulated, in part, by the SrrAB two-component regulatory system (TCRS). In the current study, we report that the SaeRS TCRS also governs fermentative biofilm formation by positively influencing AtlA activity. The SaeRS-modulated factor fibronectin-binding protein A (FnBPA) also contributed to the fermentative biofilm formation phenotype. SaeRS-dependent biofilm formation occurred in response to changes in cellular respiratory status. Genetic evidence presented suggests that a high cellular titer of phosphorylated SaeR is required for biofilm formation. Epistasis analyses found that SaeRS and SrrAB influence biofilm formation independently of one another. Analyses using a mouse model of orthopedic implant-associated biofilm formation found that both SaeRS and SrrAB govern host colonization. Of these two TCRSs, SrrAB was the dominant system driving biofilm formation in vivo. We propose a model wherein impaired cellular respiration stimulates SaeRS via an as yet undefined signal molecule(s), resulting in increasing expression of AtlA and FnBPA and biofilm formation.

scholarly journals Genetic and Biochemical Analysis of CodY-Mediated Cell Aggregation in Staphylococcus aureus Reveals an Interaction between Extracellular DNA and Polysaccharide in the Extracellular Matrix

2020 ◽  
Vol 202 (8) ◽  
Author(s):  
Kevin D. Mlynek ◽  
Logan L. Bulock ◽  
Carl J. Stone ◽  
Luke J. Curran ◽  
Marat R. Sadykov ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Surface ◽  
Biofilm Formation ◽  
Biochemical Analysis ◽  
Cell Aggregation ◽  
Extracellular Dna ◽  
Dependent Manner ◽  
Content Type ◽  
Mutant Cells

ABSTRACT The global regulator CodY links nutrient availability to the regulation of virulence factor gene expression in Staphylococcus aureus, including many genes whose products affect biofilm formation. Antithetical phenotypes of both biofilm deficiency and accumulation have been reported for codY-null mutants; thus, the role of CodY in biofilm development remains unclear. codY mutant cells of a strain producing a robust biofilm elaborate proaggregation surface-associated features not present on codY mutant cells that do not produce a robust biofilm. Biochemical analysis of the clinical isolate SA564, which aggregates when deficient for CodY, revealed that these features are sensitive to nuclease treatment and are resistant to protease exposure. Genetic analyses revealed that disrupting lgt (the diacylglycerol transferase gene) in codY mutant cells severely weakened aggregation, indicating a role for lipoproteins in the attachment of the biofilm matrix to the cell surface. An additional and critical role of IcaB in producing functional poly-N-acetylglucosamine (PIA) polysaccharide in extracellular DNA (eDNA)-dependent biofilm formation was shown. Moreover, overproducing PIA is sufficient to promote aggregation in a DNA-dependent manner regardless of source of nucleic acids. Taken together, our results point to PIA synthesis as the primary determinant of biofilm formation when CodY activity is reduced and suggest a modified electrostatic net model for matrix attachment whereby PIA associates with eDNA, which interacts with the cell surface via covalently attached membrane lipoproteins. This work counters the prevailing view that polysaccharide- and eDNA/protein-based biofilms are mutually exclusive. Rather, we demonstrate that eDNA and PIA can work synergistically to form a biofilm. IMPORTANCE Staphylococcus aureus remains a global health concern and exemplifies the ability of an opportunistic pathogen to adapt and persist within multiple environments, including host tissue. Not only does biofilm contribute to persistence and immune evasion in the host environment, it also may aid in the transition to invasive disease. Thus, understanding how biofilms form is critical for developing strategies for dispersing biofilms and improving biofilm disease-related outcomes. Using biochemical, genetic, and cell biology approaches, we reveal a synergistic interaction between PIA and eDNA that promotes cell aggregation and biofilm formation in a CodY-dependent manner in S. aureus. We also reveal that envelope-associated lipoproteins mediate attachment of the biofilm matrix to the cell surface.

scholarly journals Activity of Gallidermin on Staphylococcus aureus and Staphylococcus epidermidis Biofilms

2012 ◽  
Vol 56 (11) ◽  
pp. 5804-5810 ◽  
Author(s):  
Jongkon Saising ◽  
Linda Dube ◽  
Anne-Kathrin Ziebandt ◽  
Supayang Piyawan Voravuthikunchai ◽  
Mulugeta Nega ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Immune System ◽  
Staphylococcus Epidermidis ◽  
Biofilm Formation ◽  
Physiological State ◽  
Dependent Manner ◽  
Persister Cells ◽  
Content Type ◽  
Killing Activity ◽  
Dose Dependent

ABSTRACTDue to their abilities to form strong biofilms,Staphylococcus aureusandStaphylococcus epidermidisare the most frequently isolated pathogens in persistent and chronic implant-associated infections. As biofilm-embedded bacteria are more resistant to antibiotics and the immune system, they are extremely difficult to treat. Therefore, biofilm-active antibiotics are a major challenge. Here we investigated the effect of the lantibiotic gallidermin on two representative biofilm-forming staphylococcal species. Gallidermin inhibits not only the growth of staphylococci in a dose-dependent manner but also efficiently prevents biofilm formation by both species. The effect on biofilm might be due to repression of biofilm-related targets, such asica(intercellular adhesin) andatl(major autolysin). However, gallidermin's killing activity on 24-h and 5-day-old biofilms was significantly decreased. A subpopulation of 0.1 to 1.0% of cells survived, comprising “persister” cells of an unknown genetic and physiological state. Like many other antibiotics, gallidermin showed only limited activity on cells within mature biofilms.

scholarly journals Antibiotics Enhance Prevention and Eradication Efficacy of Cathodic-Voltage-Controlled Electrical Stimulation against Titanium-Associated Methicillin-ResistantStaphylococcus aureusandPseudomonas aeruginosaBiofilms

mSphere ◽  
2019 ◽  
Vol 4 (3) ◽  
Author(s):  
Mary K. Canty ◽  
Lisa A. Hansen ◽  
Menachem Tobias ◽  
Sandy Spencer ◽  
Terry Henry ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Pseudomonas Aeruginosa ◽  
Electrical Stimulation ◽  
Antibiotic Treatment ◽  
Biofilm Formation ◽  
Bacterial Biofilm ◽  
Dependent Manner ◽  
Methicillin Resistant ◽  
Content Type ◽  
Cathodic Voltage

ABSTRACTPeriprosthetic joint infection (PJI) develops clinically, even with antibiotic treatment, and methicillin-resistantStaphylococcus aureus(MRSA) andPseudomonas aeruginosaare predominant causes of these infections. Due to biofilm formation, antibiotic treatment for patients with PJI can perpetuate resistance, further complicating the use of noninvasive treatments. This study evaluated cathodic-voltage-controlled electrical stimulation (CVCES) of titanium, in combination with a clinically relevant antibiotic, to synergistically prevent MRSA andP. aeruginosaPJIs by inhibiting bacterial adherence or as a treatment for eradicating established biofilms. CVCES of −1.0 V, −1.5 V, or −1.8 V (versus Ag/AgCl), with or without vancomycin for MRSA or gentamicin forP. aeruginosa, was applied to sterile titanium incubated with cultures to evaluate prevention of attachment or eradication of preestablished biofilms. Treatments were 24 h long and included open-circuit potential controls, antibiotic alone, CVCES, and CVCES plus antibiotic. Biofilm-associated and planktonic CFU were enumerated. In general, CVCES at −1.8 V alone or with antibiotic completely eradicated biofilm-associated CFU for both strains, and these parameters were also highly effective against planktonic bacteria, resulting in a >6-log reduction in MRSA and no detectable planktonicP. aeruginosa. All CFU were reduced ∼3 to 5 logs from controls for prevention CVCES plus antibiotics at −1.0 V and −1.5 V against MRSA. Remarkably, there were no detectableP. aeruginosaCFU following prevention CVCES at −1.0 V or −1.5 V with gentamicin. Our results suggest that CVCES in combination with antibiotics may be an effective approach for prevention and treatment of PJI.IMPORTANCEPeriprosthetic joint infections (PJIs) develop clinically in the presence of antibiotic therapies and are responsible for increased patient morbidity and rising health care costs. Many of these infections involve bacterial biofilm formation on orthopedic hardware, and it has been well established that these biofilms are refractory to most antibiotic treatments. Recent studies have focused on novel methods to prevent and eradicate infection. Cathodic-voltage-controlled electrical stimulation (CVCES) has previously been shown to be effective as a method for prevention and eradication of Gram-positive and Gram-negative infections. The present study revealed that the utility of CVCES for prevention and eradication of methicillin-resistantStaphylococcus aureusandPseudomonas aeruginosais enhanced in the presence of clinically relevant antibiotics. The synergistic effects of CVCES and antibiotics are effective in a magnitude-dependent manner. The results of this study indicate a promising alternative method to current PJI mitigation techniques.

scholarly journals Oxantel Disrupts Polymicrobial Biofilm Development of Periodontal Pathogens

2013 ◽  
Vol 58 (1) ◽  
pp. 378-385 ◽  
Author(s):  
Stuart Dashper ◽  
Neil O'Brien-Simpson ◽  
Sze Wei Liu ◽  
Rita Paolini ◽  
Helen Mitchell ◽  
...  
Keyword(s):  
Bone Loss ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Large Scale ◽  
Alveolar Bone ◽  
Similar Degree ◽  
Dependent Manner ◽  
Gene Products ◽  
Content Type ◽  
Biofilm Development

ABSTRACTBacterial pathogens commonly associated with chronic periodontitis are the spirocheteTreponema denticolaand the Gram-negative, proteolytic speciesPorphyromonas gingivalisandTannerella forsythia. These species rely on complex anaerobic respiration of amino acids, and the anthelmintic drug oxantel has been shown to inhibit fumarate reductase (Frd) activity in some pathogenic bacteria and inhibitP. gingivalishomotypic biofilm formation. Here, we demonstrate that oxantel inhibitedP. gingivalisFrd activity with a 50% inhibitory concentration (IC50) of 2.2 μM and planktonic growth ofT. forsythiawith a MIC of 295 μM, but it had no effect on the growth ofT. denticola. Oxantel treatment caused the downregulation of sixP. gingivalisgene products and the upregulation of 22 gene products. All of these genes are part of a regulon controlled by heme availability. There was no large-scale change in the expression of genes encoding metabolic enzymes, indicating thatP. gingivalismay be unable to overcome Frd inhibition. Oxantel disrupted the development of polymicrobial biofilms composed ofP. gingivalis,T. forsythia, andT. denticolain a concentration-dependent manner. In these biofilms, all three species were inhibited to a similar degree, demonstrating the synergistic nature of biofilm formation by these species and the dependence ofT. denticolaon the other two species. In a murine alveolar bone loss model of periodontitis oxantel addition to the drinking water ofP. gingivalis-infected mice reduced bone loss to the same level as the uninfected control.

scholarly journals XerC Contributes to Diverse Forms of Staphylococcus aureus Infection viaagr-Dependent andagr-Independent Pathways

2016 ◽  
Vol 84 (4) ◽  
pp. 1214-1225 ◽  
Author(s):  
Danielle N. Atwood ◽  
Karen E. Beenken ◽  
Allister J. Loughran ◽  
Daniel G. Meeker ◽  
Tamara L. Lantz ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Biofilm Formation ◽  
Protein A ◽  
Limited Capacity ◽  
Alpha Toxin ◽  
Extracellular Proteases ◽  
Internal Organs ◽  
Content Type ◽  
Aureus Infection

We demonstrate that mutation ofxerC, which reportedly encodes a homologue of anEscherichia colirecombinase, limits biofilm formation in the methicillin-resistantStaphylococcus aureusstrain LAC and the methicillin-sensitive strain UAMS-1. This was not due to the decreased production of the polysaccharide intracellular adhesin (PIA) in either strain because the amount of PIA was increased in a UAMS-1xerCmutant and undetectable in both LAC and its isogenicxerCmutant. Mutation ofxerCalso resulted in the increased production of extracellular proteases and nucleases in both LAC and UAMS-1, and limiting the production of either class of enzymes increased biofilm formation in the isogenicxerCmutants. More importantly, the limited capacity to form a biofilm was correlated with increased antibiotic susceptibility in both strains in the context of an established biofilmin vivo. Mutation ofxerCalso attenuated virulence in a murine bacteremia model, as assessed on the basis of the bacterial loads in internal organs and overall lethality. It also resulted in the decreased accumulation of alpha toxin and the increased accumulation of protein A. These findings suggest thatxerCmay impact the functional status ofagr. This was confirmed by demonstrating the reduced accumulation of RNAIII and AgrA in LAC and UAMS-1xerCmutants. However, this cannot account for the biofilm-deficient phenotype ofxerCmutants because mutation ofagrdid not limit biofilm formation in either strain. These results demonstrate thatxerCcontributes to biofilm-associated infections and acute bacteremia and that this is likely due toagr-independent and -dependent pathways, respectively.

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