Identification of novel cytolytic peptides as key virulence determinants for community-associated MRSA
By Rong Wang, K. Braughton, Dorothee Kretschmer, T. Bach, S. Queck, Min Li, A. Kennedy, D. Dorward, S. Klebanoff, A. Peschel and 2 more. Nature Medicine, 2007
1,064 citations recorded by the source corpus.
Subfields: Infectious Diseases, Molecular Biology, Public Health, Environmental and Occupational Health
View Paper: https://www.semanticscholar.org/paper/6af6d49b0bb23e7460b079bd5811236a5cafef1f
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Infectious Diseases
- Victor J. Torres
- M. Otto
- Francis Alonzo
- F. Lowy
- R. Gordon
- Justin S. Bae
- Gordon Y C Cheung
- Tamara Reyes-Robles
In Molecular Biology
- M. Otto
- Victor J. Torres
- Francis Alonzo
- R. Gordon
- F. Lowy
- Tamara Reyes-Robles
- B. Sinha
- Robert S. Daum
In Public Health, Environmental and Occupational Health
- Gordon Y C Cheung
- M. Otto
- Justin S. Bae
- Victor J. Torres
- R. Gordon
- Robert S. Daum
- Michael Z. David
- F. Lowy
Citations in the corpus
- Intracellular staphylococcus aureus: Live-in and let die (2012, positive): “Whereas gain of function assays demonstrated PSMβ activity in phagosomal escape (Giese et al., 2011), in vivo studies suggests a prominent role of PSMα, with the third ORF of the operon, PSMα3, being the most virulent principle (Wang et al., 2007).”
- A Field Guide to Pandemic, Epidemic and Sporadic Clones of Methicillin-Resistant Staphylococcus aureus (2011, background): “ST59/952-MRSA-VT is a common and clinically important MRSA strain in Taiwan [14;128-131].”
- Staphylococcus epidermidis – the “accidental” pathogen (2009, background): “aureus PSMs, for which host defence triggering activity has been confirme”
- Characterization of a new cytotoxin that contributes to Staphylococcus aureus pathogenesis (2010, background): “These cytolytic peptides are associated with CA-MRSA virulence and have been shown to contribute significantly to human PMN lysis (Wang et al., 2007; Hongo et al., 2009).”
- Community-Associated Methicillin-Resistant Staphylococcus aureus: Epidemiology and Clinical Consequences of an Emerging Epidemic (2010, background): “These experiments suggested that PSMs may be in part responsible for the virulence of successful CA-MRSA clones (231, 980).”
- How Staphylococcus aureus biofilms develop their characteristic structure (2012, background): “In vivo, the contribution of the different PSMs todissemination seemedadditive, possibly as a result of at least the PSMα and δ-toxin having additional properties, such as the capacity to lyse red and white blood cells (14).”
- Evolution of hypervirulence by a MRSA clone through acquisition of a transposable element (2014, background): “Nonetheless, it is now clear that differences in the regulation of virulence genes also play an important role (Wang et al., 2007).”
- Staphylococcus aureus Elaborates Leukocidin AB To Mediate Escape from within Human Neutrophils (2013, background): “Phenol-soluble modulins (PSMs) have been shown to play a role in USA300 cytotoxicity (9), but it is unlikely that the residual cytotoxicity observed in the USA300 lukAB pvl double mutant is attributed to PSMs, as these cytolytic peptides would be neutralized by the serum present in this assay (38).”
- Cross‐talk between Staphylococcus aureus leukocidins‐intoxicated macrophages and lung epithelial cells triggers chemokine secretion in an inflammasome‐dependent manner (2012, background): “ity on human neutrophils when combined with PVL (Wang et al., 2007; Ventura et al., 2010).”
- Pathogenesis of methicillin-resistant Staphylococcus aureus infection. (2008, background): “[20] recently discovered that phenol-soluble modulins, a previously”
- Rapid Neutrophil Destruction following Phagocytosis of Staphylococcus aureus (2010, background): “Thus, the ability of USA300 and USA400 strains to cause relatively rapid destruction of neutrophils after phagocytosis may be linked in part to the observed high-virulence phenotype of CA-MRSA. As such, we investigated the mechanism used by USA300 to cause neutrophil destruction after phagocytosis.C”