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Staphylococcus aureus strain:multilocus sequence type 8

ABSTRACT: Fournier's gangrene caused by Panton-Valentine leukocidin-negative methicillin-sensitive Staphylococcus aureus ST8 in Japan

PROVIDER: PRJDB8899 | ENA |

REPOSITORIES: ENA

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Panton-Valentine Leukocidin Does Not Impact Virulence of Community-associated MRSA

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Project description:Panton-Valentine Leukocidin-positive Methicillin-resistant Staphylococcus aureus in Saxony, Germany, 2019

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Comparison of S. aureus PVL-positive and PVL-negative isogenic strains in exponential and stationary phase of growth

Project description:The Staphylococcus aureus Panton Valentine leukocidin (PVL) is a pore-forming toxin secreted by strains epidemiologically associated with the current outbreak of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) and with the often lethal necrotizing pneumonia. To investigate the role of PVL in pulmonary disease, we tested the pathogenicity of clinical isolates, isogenic PVL-negative and PVL-positive S. aureus strains, as well as purified PVL, in a mouse acute pneumonia model. Here we show that PVL is sufficient to cause pneumonia and that the expression of this leukotoxin induces global changes in transcriptional levels of genes encoding secreted and cell-wall-anchored staphylococcal proteins, including the lung inflammatory factor staphylococcal protein A (Spa). Keywords: comparative transcription profile in the presence or absence of PVL toxin

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Characterization and comparison of two epidemic community-associated methicillin resistant Staphylococcus aureus clones of ST59 lineage

Project description:Comparing two subclones (Taiwan clone and Asian-Pacific clone) of CA-MRSA ST59. The Taiwan clone carries the Panton-Valentine leukocidin (PVL) genes, the staphylococcal chromosomal cassette mec (SCCmec) VT and is frequently isolated from patients with severe disease. The Asian-Pacific clone is PVL-negative, carries SCCmec IV, and is a frequent colonizer of healthy children.

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A point mutation in the agr locus caused previously reported phenotypes in Staphylococcus aureus pneumonia

Project description:The role of Panton‐Valentine leukocidin (PVL) in Staphylococcus aureus pathogenesis is controversial. Here, we show that an unintended point mutation in the agr P2 promoter of S.aureus caused the phenotypes in gene regulation and murine pneumonia attributed to PVL by Labandeira‐Rey et al. (Science 315:1130‐3, 2007). In agreement with previous studies that failed to detect similar effects of PVL using community‐associated methicillin‐resistant S. aureus strains, we found no significant impact of PVL on gene expression or pathogenesis after we repaired the mutation. These findings further contribute to the idea that PVL does not have a major impact on S. aureus pathogenesis and resolve debate about its role in murine infection models. Moreover, our results demonstrate that a single nucleotide polymorphism in an intergenic region can dramatically impact bacterial physiology and virulence. Finally, our work emphasizes the need to frequently evaluate the integrity of the S. aureus agr locus.

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Panton-Valentine Leukocidin Does Not Impact Virulence of Community-associated MRSA

Project description:Panton-valentine leukocidin (PVL) has been linked to worldwide emergence of community-associated methicillin resistant Staphylococcus aureus (CA-MRSA) -- its role in virulence in unclear. Here we show that PVL had no effect on global gene expression of prominent CA-MRSA strains nor did it affect bacterial clearance from lungs, spleen and kidneys in a highly discriminatory rabbit bacteremia model. These findings negate a large body of epidemiological research that implicated PVL in CA-MRSA virulence. Keywords: mutant vs wild type in 2 different growth phases grown in 2 different medias Wild type USA 300 (strain SF8300), wild type USA 400 (strain MW2) were compared against their respective PVL isogenic knock out strains. Strains were compared at both mid-exponential and stationary phase and grown in both TSB and CCY to determine if PVL plays a role in gene regulation under these conditions.

2010-06-19 | E-GEOD-8677 | biostudies-arrayexpress

Staphylococcus aureus

Project description:Panton-Valentine Leukocidin Does Not Impact Virulence of Community-associated MRSA

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WGS of Panton-Valentine leucocidin methicillin-resistant Staphylococcus aureus

Project description:WGS of Panton-Valentine leucocidin methicillin-resistant Staphylococcus aureus

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Sublytic concentrations of Staphylococcus aureus Panton-Valentine leukocidin alter human polymorphonuclear leukocyte gene expression and enhance bactericidal capacity.

Project description:Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) infections are often caused by strains encoding Panton-Valentine leukocidin (PVL). PVL can cause lysis of polymorphonuclear leukocytes (PMNs) and other myeloid cells in vitro, a function considered widely as the primary means by which PVL might contribute to disease. However, at sublytic concentrations PVL can function as a PMN agonist. To better understand this phenomenon, we investigated the ability of PVL to alter human PMN function. PMNs exposed to PVL had enhanced capacity to produce superoxide in response to N-formyl-methionyl-leucyl-phenylalanine (fMLF), but unlike priming by lipopolysaccharide, this response did not require Toll-like receptor signal transduction. On the other hand, there was subcellular redistribution of NADPH oxidase components in PMNs following exposure of these cells to PVL - a finding consistent with priming. Priming of PMNs with other agonists such as IL-8 or GM-CSF altered the ability PVL to cause formation of pores in the plasma membranes of these cells. Microarray analysis revealed significant changes in the human PMN transcriptome following exposure to PVL, including up-regulation of molecules that regulate the inflammatory response. Consistent with the microarray data, mediators of the inflammatory response were released from PMNs after stimulation with PVL. We conclude that exposure of human PMNs to sublytic concentrations of PVL elicits a proinflammatory response that is regulated in part at the level of gene expression. We propose that PVL-mediated priming of PMNs enhances the host innate immune response. time series of PMN's non treated vs PVL treated vs iPVL treated

2012-09-06 | E-GEOD-33939 | biostudies-arrayexpress

Neutrophils from patients with recurring Panton-Valentine Leukocidin-positive Staphylococcus aureus infections are more sensitive to PVL induced NETosis

Project description:Panton-Valentine Leukocidin (PVL) is a Staphylococcus aureus toxin that binds to and kills human neutrophils resulting in the formation of neutrophil extracellular traps. A subset of individuals colonized with PVL expressing S. aureus suffer from recurring infections. We found that neutrophils from affected individuals display increased spontaneous NET formation after isolation, and increased sensitivity to killing by PVL. Compared to healthy controls, the expression of the target receptors for PVL, CD45 and C5L2, but not CD88, was increased in these patients, and the expression correlated to the amount of PVL-induced NETs produced. NADPH-oxidase activity was not important for PVL induced NETosis as neutrophils from CGD patients produced NETs in response to PVL. Through NET proteome analysis we identified that the protein content of PVL induced NETs is different from mitogen induced NETs. The abundance of the antimicrobial proteins LL37, myeloperoxidase, azurocidin, and proteinase 3 was lower on PVL NETs and PVL-induced NETs were deficient in killing Staphylococcus aureus. Neutrophils from patients that suffer from recurring PVL-positive infections may be more sensitive to PVL-induced NETosis, impairing their ability to combat the infection.

2023-11-23 | PXD025702 | Pride

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