scholarly journals Comparative Analysis of the Roles of HtrA-Like Surface Proteases in Two Virulent Staphylococcus aureus Strains

2005 ◽  
Vol 73 (1) ◽  
pp. 563-572 ◽  
Author(s):  
Candice Rigoulay ◽  
José M. Entenza ◽  
David Halpern ◽  
Eleonora Widmer ◽  
Philippe Moreillon ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Rat Model ◽  
Stress Protein ◽  
Bacterial Survival ◽  
Slight Effect ◽  
Induced Stress ◽  
Bacterial Dissemination ◽  
Virulent Strains ◽  
Stress Survival ◽  
Insertion Mutants

ABSTRACT The HtrA surface protease is involved in the virulence of many pathogens, mainly by its role in stress resistance and bacterial survival. Staphylococcus aureus encodes two putative HtrA-like proteases, referred to as HtrA1 and HtrA2. To investigate the roles of HtrA proteins in S. aureus, we constructed htrA 1, htrA 2, and htrA 1 htrA 2 insertion mutants in two genetically different virulent strains, RN6390 and COL. In the RN6390 context, htrA 1 inactivation resulted in sensitivity to puromycin-induced stress. The RN6390 htrA 1 htrA 2 mutant was affected in the expression of several secreted virulence factors comprising the agr regulon. This observation was correlated with the disappearance of the agr RNA III transcript in the RN6390 htrA 1 htrA 2 mutant. The virulence of this mutant was diminished in a rat model of endocarditis. In the COL context, both HtrA1 and HtrA2 were essential for thermal stress survival. However, only HtrA1 had a slight effect on exoprotein expression. The htrA mutations did not diminish the virulence of the COL strain in the rat model of endocarditis. Our results indicate that HtrA proteins have different roles in S. aureus according to the strain, probably depending on specific differences in the regulation of virulence factor and stress protein expression. We propose that HtrA1 and HtrA2 contribute to pathogenicity by controlling the production of certain extracellular factors that are crucial for bacterial dissemination, as revealed in the RN6390 background. We speculate that HtrA proteins act in the agr-dependent regulation pathway by assuring folding and/or maturation of some surface components of the agr system.

scholarly journals Ethanol-induced stress response of Staphylococcus aureus

2017 ◽  
Vol 63 (9) ◽  
pp. 745-757 ◽  
Author(s):  
Jasmine M. Pando ◽  
Richard F. Pfeltz ◽  
Jesus A. Cuaron ◽  
Vijayaraj Nagarajan ◽  
Mukti N. Mishra ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Stress Response ◽  
Protein Quality ◽  
Transcriptional Profiling ◽  
Stress Protein ◽  
Nucleotide Biosynthesis ◽  
Induced Stress ◽  
Stress Functions ◽  
Response Systems ◽  
Mrsa Strains

Transcriptional profiles of 2 unrelated clinical methicillin-resistant Staphylococcus aureus (MRSA) isolates were analyzed following 10% (v/v) ethanol challenge (15 min), which arrested growth but did not reduce viability. Ethanol-induced stress (EIS) resulted in differential gene expression of 1091 genes, 600 common to both strains, of which 291 were upregulated. With the exception of the downregulation of genes involved with osmotic stress functions, EIS resulted in the upregulation of genes that contribute to stress response networks, notably those altered by oxidative stress, protein quality control in general, and heat shock in particular. In addition, genes involved with transcription, translation, and nucleotide biosynthesis were downregulated. relP, which encodes a small alarmone synthetase (RelP), was highly upregulated in both MRSA strains following ethanol challenge, and relP inactivation experiments indicated that this gene contributed to EIS growth arrest. A number of persistence-associated genes were also upregulated during EIS, including those that encode toxin–antitoxin systems. Overall, transcriptional profiling indicated that the MRSA investigated responded to EIS by entering a state of dormancy and by altering the expression of elements from cross protective stress response systems in an effort to protect preexisting proteins.

Staphylococcus aureus ClpYQ plays a minor role in stress survival

2005 ◽  
Vol 183 (4) ◽  
pp. 286-291 ◽  
Author(s):  
Dorte Frees ◽  
Line E. Thomsen ◽  
Hanne Ingmer
Keyword(s):  
Staphylococcus Aureus ◽  
Minor Role ◽  
Stress Survival ◽  
A Minor

Coating with a novel gentamicinpalmitate formulation prevents implant-associated osteomyelitis induced by methicillin-susceptible Staphylococcus aureus in a rat model

2014 ◽  
Vol 39 (5) ◽  
pp. 981-988 ◽  
Author(s):  
Christian Fölsch ◽  
Maike Federmann ◽  
Klaus D. Kuehn ◽  
Clemens Kittinger ◽  
Stefan Kogler ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Rat Model

scholarly journals Attieké street vendors: a potential source for dissemination of virulent strains of Staphylococcus aureus in consumers

2019 ◽  
Vol 13 (3) ◽  
pp. 1420
Author(s):  
Sylvie Mireille Kouamé-Sina ◽  
Yakoura K. Ouattara ◽  
Fernique Konan ◽  
David Coulibaly N’golo ◽  
Kan Stephane Kouassi ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Street Vendors ◽  
Potential Source ◽  
Virulent Strains

scholarly journals Is intracellular Staphylococcus aureus associated with recurrent infection in a rat model of open fracture?

2020 ◽  
Vol 9 (2) ◽  
pp. 71-76
Author(s):  
Tao Gao ◽  
Junqing Lin ◽  
Changqing Zhang ◽  
Hongyi Zhu ◽  
Xianyou Zheng
Keyword(s):  
Staphylococcus Aureus ◽  
Bone Marrow ◽  
Green Fluorescent Protein ◽  
Rat Model ◽  
Open Fracture ◽  
Fluorescent Protein ◽  
Kirschner Wire ◽  
Recurrent Infection ◽  
Host Immune System ◽  
Green Fluorescent

Aims The purpose of this study was to determine whether intracellular Staphylococcus aureus is associated with recurrent infection in a rat model of open fracture. Methods After stabilizing with Kirschner wire, we created a midshaft femur fracture in Sprague-Dawley rats and infected the wound with green fluorescent protein (GFP)-tagged S. aureus. After repeated debridement and negative swab culture was achieved, the isolation of GFP-containing cells from skin, bone marrow, and muscle was then performed. The composition and viability of intracellular S. aureus in isolated GFP-positive cells was assessed. We suppressed the host immune system and observed whether recurrent infection would occur. Finally, rats were assigned to one of six treatment groups (a combination of antibiotic treatment and implant removal/retention). The proportion of successful eradication was determined. Results Green fluorescent protein-containing cells were successfully isolated after the swab culture was negative from skin (n = 0, 0%), muscle (n = 10, 100%), and bone marrow (n = 10, 100%) of a total of ten rats. The phagocytes were predominant in GFP-positive cells from muscle (73%) and bone marrow (81%) with a significantly higher viability of intracellular S. aureus (all p-values < 0.001). The recurrent infection occurred in up to 75% of rats after the immunosuppression. The proportion of successful eradication was not associated with implant retention or removal, and the efficacy of linezolid in eradicating intracellular S. aureus is significantly higher than that of vancomycin. Conclusion Intracellular S. aureus is associated with recurrent infection in the rat model of open fracture. Usage of linezolid, a membrane-permeable antibiotic, is an effective strategy against intracellular S. aureus. Cite this article: Bone Joint Res. 2020;9(2):71–76.

scholarly journals Virulence of methicillin-resistant Staphylococcus aureus modulated by the YycFG two-component pathway in a rat model of osteomyelitis

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Shizhou Wu ◽  
Yunjie Liu ◽  
Lei Lei ◽  
Hui Zhang
Keyword(s):  
Staphylococcus Aureus ◽  
Western Blot ◽  
Rat Model ◽  
Biofilm Formation ◽  
Bacterial Biofilm ◽  
Invasive Ability ◽  
Methicillin Resistant ◽  
Two Component ◽  
Mrsa Strains

Abstract Objectives Methicillin-resistant Staphylococcus aureus (MRSA) strains present an urgent medical problem in osteomyelitis cases. Our previous study indicated that the YycFG two-component regulatory pathway is associated with the bacterial biofilm organization of MRSA strains. The aim of this study was to investigate the regulatory roles of ASyycG in the bacterial biofilm formation and the pathogenicity of MRSA strains using an antisense RNA strategy. Methods An ASyycG-overexpressing MRSA clinical isolate was constructed. The bacterial growth was monitored, and the biofilm biomass on bone specimens was examined using scanning electron microscopy and confocal laser scanning microscopy. Furthermore, quantitative RT-PCR (QRT-PCR) analysis was used to measure the expression of yycF/G/H and icaA/D in the MRSA and ASyycG strains. The expression of the YycG protein was quantified by Western blot assays. We validated the role of ASyycG in the invasive ability and pathogenicity of the strains in vivo using histology and peptide nucleic acid fluorescent in situ hybridization. Results The results showed that overexpression of ASyycG lead to a reduction in biofilm formation and exopolysaccharide (EPS) synthesis compared to the control MRSA strains. The ASyycG strains exhibited decreased expression of the yycF/G/H and icaA/D genes. Furthermore, Western blot data showed that the production of the YycG protein was inhibited in the ASyycG strains. In addition, we demonstrated that ASyycG suppressed the invasive ability and pathogenicity of the strain in vivo using an SPF (specific pathogen free) rat model. Conclusion In summary, the overexpression of ASyycG leads to a reduction in biofilm formation and bacterial pathogenicity in vivo, which provides a potential target for the management of MRSA-induced osteomyelitis.

scholarly journals Antimicrobial Peptide Induced-Stress Renders Staphylococcus aureus Susceptible to Toxic Nucleoside Analogs

2020 ◽  
Vol 11 ◽  
Author(s):  
Alexandro Rodríguez-Rojas ◽  
Arpita Nath ◽  
Baydaa El Shazely ◽  
Greta Santi ◽  
Joshua Jay Kim ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Antimicrobial Peptide ◽  
Nucleoside Analogs ◽  
Induced Stress

scholarly journals Increased Virulence of a Fibronectin-Binding Protein Mutant of Staphylococcus aureus in a Rat Model of Pneumonia

2002 ◽  
Vol 70 (7) ◽  
pp. 3865-3873 ◽  
Author(s):  
Mary C. McElroy ◽  
David J. Cain ◽  
Christine Tyrrell ◽  
Timothy J. Foster ◽  
Christopher Haslett
Keyword(s):  
Staphylococcus Aureus ◽  
Epithelial Cells ◽  
Rat Model ◽  
Binding Proteins ◽  
Binding Protein ◽  
Alveolar Epithelial Cells ◽  
Alveolar Epithelial ◽  
Fibronectin Binding Protein ◽  
Fibronectin Binding

ABSTRACT Fibronectin-binding proteins mediate Staphylococcus aureus internalization into nonphagocytic cells in vitro. We have investigated whether fibronectin-binding proteins are virulence factors in the pathogenesis of pneumonia by using S. aureus strain 8325-4 and isogenic mutants in which fibronectin-binding proteins were either deleted (DU5883) or overexpressed [DU5883(pFnBPA4)]. We first demonstrated that fibronectin-binding proteins mediate S. aureus internalization into alveolar epithelial cells in vitro and that S. aureus internalization into alveolar epithelial cells requires actin rearrangement and protein kinase activity. Second, we established a rat model of S. aureus-induced pneumonia and measured lung injury and bacterial survival at 24 and 96 h postinoculation. S. aureus growth and the extent of lung injury were both increased in rats inoculated with the deletion mutant (DU5883) in comparison with rats inoculated with the wild-type (8325-4) and the fibronectin-binding protein-overexpressing strain DU5883(pFnBPA4) at 24 h postinfection. Morphological evaluation of infected lungs at the light and electron microscopic levels demonstrated that S. aureus was present within neutrophils from both 8325-4- and DU5883-inoculated lungs. Our data suggest that fibronectin-binding protein-mediated internalization into alveolar epithelial cells is not a virulence mechanism in a rat model of pneumonia. Instead, our data suggest that fibronectin-binding proteins decrease the virulence of S. aureus in pneumonia.

scholarly journals Staphylococcus aureus biofilms release leukocidins to elicit extracellular trap formation and evade neutrophil-mediated killing

2018 ◽  
Vol 115 (28) ◽  
pp. 7416-7421 ◽  
Author(s):  
Mohini Bhattacharya ◽  
Evelien T. M. Berends ◽  
Rita Chan ◽  
Elizabeth Schwab ◽  
Sashwati Roy ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
White Blood Cells ◽  
Neutrophil Extracellular Trap ◽  
Bacterial Survival ◽  
Chronic Infections ◽  
Burn Wound ◽  
Wound Model ◽  
Immune Defenses ◽  
Extracellular Trap

Bacterial biofilms efficiently evade immune defenses, greatly complicating the prognosis of chronic infections. How methicillin-resistant Staphylococcus aureus (MRSA) biofilms evade host immune defenses is largely unknown. This study describes some of the major mechanisms required for S. aureus biofilms to evade the innate immune response and provides evidence of key virulence factors required for survival and persistence of bacteria during chronic infections. Neutrophils are the most abundant white blood cells in circulation, playing crucial roles in the control and elimination of bacterial pathogens. Specifically, here we show that, unlike single-celled populations, S. aureus biofilms rapidly skew neutrophils toward neutrophil extracellular trap (NET) formation through the combined activity of leukocidins Panton–Valentine leukocidin and γ-hemolysin AB. By eliciting this response, S. aureus was able to persist, as the antimicrobial activity of released NETs was ineffective at clearing biofilm bacteria. Indeed, these studies suggest that NETs could inadvertently potentiate biofilm infections. Last, chronic infection in a porcine burn wound model clearly demonstrated that leukocidins are required for “NETosis” and facilitate bacterial survival in vivo.

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