Relevant bibliographies by topics / Phenol-soluble modulins (PSM)

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

Author: Grafiati
Published: 4 June 2021
Last updated: 10 February 2022

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

1

Cheung, Gordon Y. C., Dorothee Kretschmer, Shu Y. Queck, Hwang‐Soo Joo, Rong Wang, Anthony C. Duong, Thuan H. Nguyen, et al. "Insight into structure‐function relationship in phenol‐soluble modulins using an alanine screen of the phenol‐soluble modulin (PSM) α3 peptide." FASEB Journal 28, no. 1 (September 5, 2013): 153–61. http://dx.doi.org/10.1096/fj.13-232041.

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Dastgheyb, Sana S., Amer E. Villaruz, Katherine Y. Le, Vee Y. Tan, Anthony C. Duong, Som S. Chatterjee, Gordon Y. C. Cheung, Hwang-Soo Joo, Noreen J. Hickok, and Michael Otto. "Role of Phenol-Soluble Modulins in Formation of Staphylococcus aureus Biofilms in Synovial Fluid." Infection and Immunity 83, no. 7 (May 11, 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 exceptional dimensions. Our results indicate that PSMs function by disrupting interactions of biofilm matrix molecules, such as the polysaccharide intercellular adhesin (PIA), with the bacterial cell surface. Together, our findings support a two-step model of staphylococcal prosthetic joint infection: As we previously reported, interaction ofS. aureussurface proteins with host matrix proteins such as fibrin initiates agglomeration; our present results show that, thereafter, the bacterial agglomerates grow to extremely large sizes owing to the lack of PSM expression under the specific conditions present in joints. Our findings provide a mechanistic explanation for the reported extreme resistance of joint infection to antibiotic treatment, lend support to the notions that Agr functionality and PSM production play a major role in defining different forms ofS. aureusinfection, and have important implications for antistaphylococcal therapeutic strategies.
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Deplanche, Martine, Ludmila Alekseeva, Ksenia Semenovskaya, Chih-Lung Fu, Frederic Dessauge, Laurence Finot, Wolfram Petzl, et al. "Staphylococcus aureus Phenol-Soluble Modulins Impair Interleukin Expression in Bovine Mammary Epithelial Cells." Infection and Immunity 84, no. 6 (March 21, 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 modulin (PSM) peptides as key contributors to these effects, as IL-32, IL-6, and IL-8 expression by epithelial cells exposed topsmmutant strains was significantly increased compared to that in cells exposed to the isogenicS. aureuswild-type strain, indicating that PSMs inhibit the production of these interleukins. The use of genetically complemented strains confirmed this observation. Inasmuch as the decreased expression of IL-32, which is involved in dendritic cell maturation, impairs immune responses, our results support a PSM-dependent mechanism that allows for the development of chronicS. aureus-related mastitis.
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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 (January 7, 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 individual PSMs under different conditions. We established that there is a pH-induced switch in PSM aggregation kinetics. Different lag times and growth of fibrils were observed, which indicates that there was no clear correlation between the rates of fibril elongation among different PSMs. This finding confirms that pH can modulate the aggregation properties of these peptides and suggest a deeper understanding of the formation of aggregates, which represents an important basis for strategies to interfere and might help in reducing the risk of biofilm-related infections.
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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 (June 13, 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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Tsompanidou, Eleni, Emma L. Denham, Dörte Becher, Anne de Jong, Girbe Buist, Marleen van Oosten, Willem L. Manson, Jaap Willem Back, Jan Maarten van Dijl, and Annette Dreisbach. "Distinct Roles of Phenol-Soluble Modulins in Spreading of Staphylococcus aureus on Wet Surfaces." Applied and Environmental Microbiology 79, no. 3 (November 26, 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 produced byS. aureus, these peptides were chemically synthesized and tested in spreading assays with differentpsmmutant strains. The results show that PSMα3 and PSMγ are the strongest facilitators of spreading both for planktonic cells and cells in catheter-associated biofilms. Compared to the six other PSMs ofS. aureus, PSMα3 and PSMγ combine strong surfactant activities with a relatively low overall hydropathicity. Importantly, we show that PSM-mediated motility ofS. aureusfacilitates the rapid colonization of wet surfaces next to catheters and the colonization of fresh meat.
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Zeytuni, N., S. W. Dickey, J. Hu, H. T. Chou, L. J. Worrall, J. A. N. Alexander, M. L. Carlson, et al. "Structural insight into the Staphylococcus aureus ATP-driven exporter of virulent peptide toxins." Science Advances 6, no. 40 (September 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 crystallography. We have captured the transporter in the ATP-bound state at near atomic resolution, revealing a type II ABC exporter fold, with an additional cytosolic domain. Comparison to a lower-resolution nucleotide-free map displaying an “open” conformation and putative hydrophobic inner chamber of a size able to accommodate the binding of two PSM peptides provides mechanistic insight and sets the foundation for therapeutic design.
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Kim, Deok-ryeong, Yeonhee Lee, Hyeon-kyeong Kim, Wooseong Kim, Yun-Gon Kim, Yung-Hun Yang, Jae-Seok Kim, and Hwang-Soo Joo. "Phenol-Soluble Modulin-Mediated Aggregation of Community-Associated Methicillin-Resistant Staphylococcus Aureus in Human Cerebrospinal Fluid." Cells 9, no. 3 (March 24, 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 strain, USA300 LAC, and incubated overnight. Cell aggregation images were acquired after culture and image analysis was performed. The cell aggregation ratio in WT samples differed significantly between the two sampling sites (intraventricular: 0.2% vs. lumbar intrathecal: 6.7%, p < 0.001). The cell aggregation ratio in Δpsm samples also differed significantly between the two sampling sites (intraventricular: 0.0% vs. lumbar intrathecal: 1.2%, p < 0.001). Division of the study cases into two groups according to the aggregated area ratio (WT/Δpsm; group A: ratio of ≥ 2, group B: ratio of < 2) showed that the median aggregation ratio value differed significantly between groups A and B (5.5 and 0, respectively, p < 0.001). The differences in CSF distribution and PSM presence within the specific CSF environment are significant factors affecting bacterial cell aggregation.
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Schwartz, Kelly, Matthew D. Sekedat, Adnan K. Syed, Brendan O'Hara, David E. Payne, Abigail Lamb, and Blaise R. Boles. "The AgrD N-Terminal Leader Peptide of Staphylococcus aureus Has Cytolytic and Amyloidogenic Properties." Infection and Immunity 82, no. 9 (June 30, 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-AgrD) beyond AgrD propeptide trafficking has never been described before. We observe that N-AgrD, like the PSMs, is found in the amyloid fibrils ofS. aureusbiofilms and is capable of forming and seeding amyloid fibrilsin vitro. N-AgrD displays cytolytic and proinflammatory properties that are abrogated after fibril formation. These data suggest that the N-AgrD leader peptide affectsS. aureusbiology in a manner similar to that described previously for the PSM peptide toxins. Taken together, our findings suggest that peptide cleavage products can affect cellular function beyond their canonical roles and may represent a class of virulence factors warranting further exploration.
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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 (June 15, 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 ofStaphylococcusare capable of causing release of interleukin 18 (IL-18) from keratinocytes and thatS. aureusPSMs are necessary and sufficient to stimulate IL-18 release from keratinocytes independently of caspase 1. Further, after 7 days of epicutaneous exposure to wild-typeS. aureus, but notS. aureusΔpsm, we saw dramatic changes in gross pathology, as well as systemic release of proinflammatory cytokines. This work demonstrates the importance of PSM peptides inS. aureus-mediated inflammatory cytokine release from keratinocytesin vitroandin vivoand further implicates PSMs as important contributors to pathogenesis.
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Dissertations / Theses on the topic "Phenol-soluble modulins (PSM)"

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Hodille, Elisabeth. "Les facteurs de virulence staphylococciques : interaction avec les mastocytes humains et modulation de leur expression par les antibiotiques." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSE1109/document.

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S. aureus est un pathogène majeur de l’Homme capable de produire une grande variété de facteurs de virulence tels que les phénol-solubles modulines alpha (PSM) et l’hémolysine delta (Hld). La transmission de S. aureus est essentiellement manu-portée mais les éléments favorisant sa dissémination dans la population restent inconnus. Les mastocytes étant connus pour libérer des médiateurs pruritogènes, nous avons suspecté leur implication dans la physiopathologie et la transmission des infections cutanées staphylococciques. Sur une lignée de mastocytes humains, l’Hld et les PSM1, montrés pour être produits in vivo, déclenchaient la libération de tels médiateurs. Chez S. aureus, la production des toxines est sous la dépendance du système de régulation globale Agr. Les souches de S. aureus appartenant au type Agr1, produisant significativement plus d’Hld et de PSM que les autres souches, ont été les plus fréquemment retrouvées au cours de l’année 2017 dans les infections cutanées staphylococciques. Ceci corrobore l’hypothèse selon laquelle une souche de S. aureus produisant des toxines capables d’interagir avec les mastocytes et induisant un prurit, diffuse plus facilement dans la population. Nous avons ensuite étudié la modulation de l’expression des PSM et d’Hld par des concentrations sub-inhibitrices d’antibiotiques. L’oxacilline induisait une inhibition de l’expression des PSM et d’Hld alors que la clindamycine entraînait plus fréquemment une induction de leur expression. Ces observations nous ont interrogé sur l’utilisation de la clindamycine considérée habituellement comme anti-toxinique et sur l’effet bénéfique ou délétère de l’effet inhibiteur de l’oxacilline
S. aureus is a major human pathogen able to produce several virulence factors such as phenol-solublemodulins alpha (PSMalpha) and delta hemolysin (Hld). S. aureus is essentially spread through hand butthe elements promoting its spreading stay unsolved. Mast cells release several soluble mediatorstriggering itching behavior. We suspect the mast cell involvement in spreading of S. aureus strains andin physiopathology of staphylococcal skin infections. Upon human mast cell line, we showed thatPSMalpha1 and Hld induced the release of mediators triggering itching behavior. Moreover, these toxinswere produced in vivo during staphylococcal skin infections. Expression of staphylococcal virulencefactors is regulated by global regulatory system Agr. Interestingly, we observed that S. aureus strainsbelonging in Agr1 produced higher quantity of PSMalpha and Hld than those belonging to Agr2 and Agr3,and were more frequently responsible to skin infections during the last year. This observation supportsour hypothesis whereby a strain producing toxins able to trigger mast cell mediator inducingscratching behavior, spreads electively in the community. Thereafter, we studied modulation of PSMalphaand Hld expression by sub-inhibitory concentration of antibiotics. We reported that oxacillin inducedan inhibitory effect on PSMalpha and Hld expression, while clindamycin resulted in more frequently aninducer effect. These results are discordant with these observed with Panton-Valentine leucocidin andalpha hemolysin and interrogate on clindamycin use for its anti-toxin activity and on benefic ordeleterious effect of oxacillin inhibitory effect
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