Academic literature on the topic 'Phenol-soluble modulins (PSM)'

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Journal articles on the topic "Phenol-soluble modulins (PSM)"

1

Cheung, Gordon Y. C., Dorothee Kretschmer, Shu Y. Queck та ін. "Insight into structure‐function relationship in phenol‐soluble modulins using an alanine screen of the phenol‐soluble modulin (PSM) α3 peptide". FASEB Journal 28, № 1 (2013): 153–61. http://dx.doi.org/10.1096/fj.13-232041.

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2

Dastgheyb, Sana S., Amer E. Villaruz, Katherine Y. Le, et al. "Role of Phenol-Soluble Modulins in Formation of Staphylococcus aureus Biofilms in Synovial Fluid." Infection and Immunity 83, no. 7 (2015): 2966–75. http://dx.doi.org/10.1128/iai.00394-15.

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Staphylococcus aureusis a leading cause of prosthetic joint infections, which, as we recently showed, proceed with the involvement of biofilm-like clusters that cause recalcitrance to antibiotic treatment. Here we analyzed why these clusters grow extraordinarily large, reaching macroscopically visible extensions (>1 mm). We found that while specificS. aureussurface proteins are a prerequisite for agglomeration in synovial fluid, low activity of the Agr regulatory system and subsequent low production of the phenol-soluble modulin (PSM) surfactant peptides cause agglomerates to grow to except
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3

Deplanche, Martine, Ludmila Alekseeva, Ksenia Semenovskaya, et al. "Staphylococcus aureus Phenol-Soluble Modulins Impair Interleukin Expression in Bovine Mammary Epithelial Cells." Infection and Immunity 84, no. 6 (2016): 1682–92. http://dx.doi.org/10.1128/iai.01330-15.

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The role of the recently described interleukin-32 (IL-32) inStaphylococcus aureus-induced mastitis, an inflammation of the mammary gland, is unclear. We determined expression of IL-32, IL-6, and IL-8 inS. aureus- andEscherichia coli-infected bovine mammary gland epithelial cells. Using live bacteria, we found that inS. aureus-infected cells, induction of IL-6 and IL-8 expression was less pronounced than inE. coli-infected cells. Notably, IL-32 expression was decreased inS. aureus-infected cells, while it was increased inE. coli-infected cells. We identified the staphylococcal phenol-soluble mo
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4

Zaman, Masihuz, and Maria Andreasen. "Modulating Kinetics of the Amyloid-Like Aggregation of S. aureus Phenol-Soluble Modulins by Changes in pH." Microorganisms 9, no. 1 (2021): 117. http://dx.doi.org/10.3390/microorganisms9010117.

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The pathogen Staphylococcus aureus is recognized as one of the most frequent causes of biofilm-associated infections. The recently identified phenol-soluble modulin (PSM) peptides act as the key molecular effectors of staphylococcal biofilm maturation and promote the formation of an aggregated fibril structure. The aim of this study was to evaluate the effect of various pH values on the formation of functional amyloids of individual PSM peptides. Here, we combined a range of biophysical, chemical kinetics and microscopic techniques to address the structure and aggregation mechanism of individu
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Yamaki, Jason, Timothy Synold, and Annie Wong-Beringer. "Antivirulence Potential of TR-700 and Clindamycin on Clinical Isolates of Staphylococcus aureus Producing Phenol-Soluble Modulins." Antimicrobial Agents and Chemotherapy 55, no. 9 (2011): 4432–35. http://dx.doi.org/10.1128/aac.00122-11.

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ABSTRACTStaphylococcus aureusstrains (n= 50) causing complicated skin and skin structure infections produced various levels of phenol-soluble modulin alpha-type (PSMα) peptides; some produced more than twice that produced by the control strain (LAC USA300). TR-700 (oxazolidinone) and clindamycin strongly inhibited PSM production at one-half the MIC but exhibited weak to modest induction at one-fourth and one-eighth the MICs, primarily in low producers. Adequate dosing of these agents is emphasized to minimize the potential for paradoxical induction of virulence.
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6

Tsompanidou, Eleni, Emma L. Denham, Dörte Becher, et al. "Distinct Roles of Phenol-Soluble Modulins in Spreading of Staphylococcus aureus on Wet Surfaces." Applied and Environmental Microbiology 79, no. 3 (2012): 886–95. http://dx.doi.org/10.1128/aem.03157-12.

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ABSTRACTThe human pathogenStaphylococcus aureusis renowned for the rapid colonization of contaminated wounds, medical implants, and food products. Nevertheless, little is known about the mechanisms that allowS. aureusto colonize the respective wet surfaces. The present studies were therefore aimed at identifying factors used byS. aureuscells to spread over wet surfaces, starting either from planktonic or biofilm-associated states. Through proteomics analyses we pinpoint phenol-soluble modulins (PSMs) as prime facilitators of the spreading process. To dissect the roles of the eight PSMs produce
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7

Zeytuni, N., S. W. Dickey, J. Hu, et al. "Structural insight into the Staphylococcus aureus ATP-driven exporter of virulent peptide toxins." Science Advances 6, no. 40 (2020): eabb8219. http://dx.doi.org/10.1126/sciadv.abb8219.

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Staphylococcus aureus is a major human pathogen that has acquired alarming broad-spectrum antibiotic resistance. One group of secreted toxins with key roles during infection is the phenol-soluble modulins (PSMs). PSMs are amphipathic, membrane-destructive cytolytic peptides that are exported to the host-cell environment by a designated adenosine 5′-triphosphate (ATP)–binding cassette (ABC) transporter, the PSM transporter (PmtABCD). Here, we demonstrate that the minimal Pmt unit necessary for PSM export is PmtCD and provide its first atomic characterization by single-particle cryo-EM and x-ray
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Kim, Deok-ryeong, Yeonhee Lee, Hyeon-kyeong Kim, et al. "Phenol-Soluble Modulin-Mediated Aggregation of Community-Associated Methicillin-Resistant Staphylococcus Aureus in Human Cerebrospinal Fluid." Cells 9, no. 3 (2020): 788. http://dx.doi.org/10.3390/cells9030788.

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Phenol-soluble modulins (PSMs) are major determinants of Staphylococcus aureus virulence and their increased production in community-associated methicillin-resistant S. aureus (CA-MRSA) likely contributes to the enhanced virulence of MRSA strains. Here, we analyzed the differences in bacterial cell aggregation according to PSM presence in the specific human cerebrospinal fluid (CSF) environment. CSF samples from the intraventricular or lumbar intrathecal area of each patient and tryptic soy broth media were mixed at a 1:1 ratio, inoculated with WT and PSM-deleted mutants (Δpsm) of the CA-MRSA
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9

Schwartz, Kelly, Matthew D. Sekedat, Adnan K. Syed, et al. "The AgrD N-Terminal Leader Peptide of Staphylococcus aureus Has Cytolytic and Amyloidogenic Properties." Infection and Immunity 82, no. 9 (2014): 3837–44. http://dx.doi.org/10.1128/iai.02111-14.

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ABSTRACTStaphylococcus aureusvirulence is coordinated through the Agr quorum-sensing system to produce an array of secreted molecules. One important class of secreted virulence factors is the phenol-soluble modulins (PSMs). PSMs are small-peptide toxins that have recently been characterized for their roles in infection, biofilm development, and subversion of the host immune system. In this work, we demonstrate that the signal peptide of theS. aureusquorum-sensing signal, AgrD, shares structural and functional similarities with the PSM family of toxins. The efficacy of this peptide (termed N-Ag
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Syed, Adnan K., Tamra J. Reed, Kaitlyn L. Clark, Blaise R. Boles, and J. Michelle Kahlenberg. "Staphlyococcus aureus Phenol-Soluble Modulins Stimulate the Release of Proinflammatory Cytokines from Keratinocytes and Are Required for Induction of Skin Inflammation." Infection and Immunity 83, no. 9 (2015): 3428–37. http://dx.doi.org/10.1128/iai.00401-15.

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Staphylococcus aureusis a human commensal that colonizes the skin. While it is normally innocuous, it has strong associations with atopic dermatitis pathogenesis and has become the leading cause of skin and soft tissue infections in the United States. The factors that dictate the role ofS. aureusin disease are still being determined. In this work, we utilized primary keratinocyte culture and an epidermal murine colonization model to investigate the role ofS. aureusphenol-soluble modulins (PSMs) in proinflammatory cytokine release and inflammation induction. We demonstrated that many species of
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