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

Author: Grafiati

Published: 4 June 2021

Last updated: 10 February 2022

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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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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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Horvatek, Petra, Andrea Salzer, Andrew Magdy Fekry Hanna, et al. "Inducible expression of (pp)pGpp synthetases in Staphylococcus aureus is associated with activation of stress response genes." PLOS Genetics 16, no. 12 (2020): e1009282. http://dx.doi.org/10.1371/journal.pgen.1009282.

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The stringent response is characterized by the synthesis of the messenger molecules pppGpp, ppGpp or pGpp (here collectively designated (pp)pGpp). The phenotypic consequences resulting from (pp)pGpp accumulation vary among species and can be mediated by different underlying mechanisms. Most genome-wide analyses have been performed under stress conditions, which often mask the immediate effects of (pp)pGpp-mediated regulatory circuits. In Staphylococcus aureus, (pp)pGpp can be synthesized via the RelA-SpoT-homolog, RelSau upon amino acid limitation or via one of the two small (pp)pGpp synthetas

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12

Monecke, Stefan, Geoffrey W. Coombs, Julie Pearson, Helmut Hotzel, Peter Slickers, and Ralf Ehricht. "A Clonal Complex 12 Methicillin-Resistant Staphylococcus aureus Strain, West Australian MRSA-59, Harbors a Novel Pseudo-SCCmecElement." Antimicrobial Agents and Chemotherapy 59, no. 11 (2015): 7142–44. http://dx.doi.org/10.1128/aac.01745-15.

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ABSTRACTA West Australian methicillin-resistantStaphylococcus aureusstrain (WA MRSA-59) was characterized by microarray and sequencing. Its pseudo-staphylococcal cassette chromosomemec(SCCmec) element compriseddcs,Q9XB68-dcs,mvaS-SCC,Q5HJW6,dru,ugpQ,ydeM,mecA-mecR-mecI, txbimecI,tnpIS431,copA2-mco(copper resistance),ydhK,arsC-arsB-arsR(arsenic resistance), open reading frame PT43, andper-2. Recombinase genes,xylR(mecR2), and PSM-mec(phenol-soluble modulin) were absent. We suggest thatmeccomplex A should be split into two subtypes. One harbors PSM-mecandxylR(mecR2). It is found in SCCmectypes I

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13

Mehlin, Christopher, Catherine M. Headley, and Seymour J. Klebanoff. "An Inflammatory Polypeptide Complex from Staphylococcus epidermidis: Isolation and Characterization." Journal of Experimental Medicine 189, no. 6 (1999): 907–18. http://dx.doi.org/10.1084/jem.189.6.907.

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Staphylococcus epidermidis releases factors that activate the HIV-1 long terminal repeat, induce cytokine release, and activate nuclear factor κB in cells of macrophage lineage. The active material had a mass of 34,500 daltons, was inactivated by proteases and partitioned into the phenol layer on hot aqueous phenol extraction, and thus was termed phenol-soluble modulin (PSM). High performance liquid chromatography (HPLC) of crude PSM yielded two peaks of activity designated PSM peak 1 and peak 2. MALDI-TOF (matrix-assisted laser desorption ionization-time of flight) mass spectroscopy indicated

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14

Laabei, Maisem, W. David Jamieson, Yi Yang, Jean van den Elsen, and A. Toby A. Jenkins. "Investigating the lytic activity and structural properties of Staphylococcus aureus phenol soluble modulin (PSM) peptide toxins." Biochimica et Biophysica Acta (BBA) - Biomembranes 1838, no. 12 (2014): 3153–61. http://dx.doi.org/10.1016/j.bbamem.2014.08.026.

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15

Berube, Bryan J., Georgia R. Sampedro, Michael Otto та Juliane Bubeck Wardenburg. "Thepsmα Locus Regulates Production of Staphylococcus aureus Alpha-Toxin during Infection". Infection and Immunity 82, № 8 (2014): 3350–58. http://dx.doi.org/10.1128/iai.00089-14.

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ABSTRACTStaphylococcus aureusis a leading cause of human bacterial infection, causing a wide spectrum of disease ranging from skin and soft tissue infections to life-threatening pneumonia and sepsis.S. aureustoxins play an essential role in disease pathogenesis, contributing to both immunomodulation and host tissue injury. Prominent among these toxins are the membrane-active pore-forming cytolysin alpha-toxin (Hla) and the amphipathic α-helical phenol-soluble modulin (PSM) peptides. As deletion of either thehlaorpsmlocus leads to a phenotypically similar virulence defect in skin and soft tissu

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Forsman, Huamei, Karin Christenson, Johan Bylund, and Claes Dahlgren. "Receptor-Dependent and -Independent Immunomodulatory Effects of Phenol-Soluble Modulin Peptides from Staphylococcus aureus on Human Neutrophils Are Abrogated through Peptide Inactivation by Reactive Oxygen Species." Infection and Immunity 80, no. 6 (2012): 1987–95. http://dx.doi.org/10.1128/iai.05906-11.

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ABSTRACTThe virulence and pathogenesis mechanisms of community-associated methicillin-resistantStaphylococcus aureus(CA-MRSA) strains depend on a newly described group of phenol-soluble modulin (PSM) peptides (the PSMα peptides) with cytolytic activity. These toxins are α-helical peptides with a formyl group at the N terminus, and they activate neutrophils through formyl peptide receptor 2 (FPR2), a function closely correlated to the capacity of staphylococcal species to cause invasive infections. The effects of two synthetic PSMα peptides were investigated, and we show that they utilize FPR2

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Gonzalez, David J., Lisa Vuong, Isaiah S. Gonzalez, et al. "Phenol Soluble Modulin (PSM) Variants of Community-Associated Methicillin-ResistantStaphylococcus aureus(MRSA) Captured Using Mass Spectrometry-Based Molecular Networking." Molecular & Cellular Proteomics 13, no. 5 (2014): 1262–72. http://dx.doi.org/10.1074/mcp.m113.031336.

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18

Chatterjee, Som S., Liang Chen, Hwang-Soo Joo, Gordon Y. C. Cheung, Barry N. Kreiswirth, and Michael Otto. "Distribution and Regulation of the Mobile Genetic Element-Encoded Phenol-Soluble Modulin PSM-mec in Methicillin-Resistant Staphylococcus aureus." PLoS ONE 6, no. 12 (2011): e28781. http://dx.doi.org/10.1371/journal.pone.0028781.

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19

Abad, Lélia, Jérôme Josse, Jason Tasse, et al. "Antibiofilm and intraosteoblastic activities of rifamycins against Staphylococcus aureus: promising in vitro profile of rifabutin." Journal of Antimicrobial Chemotherapy 75, no. 6 (2020): 1466–73. http://dx.doi.org/10.1093/jac/dkaa061.

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Abstract Background Targeting biofilm-embedded and intraosteoblastic Staphylococcus aureus, rifampicin gained a pivotal role in bone and joint infection (BJI) treatment. Two other rifamycins, rifabutin and rifapentine, may represent better-tolerated alternatives, but their activity against bacterial reservoirs associated with BJI chronicity has never been evaluated. Objectives To evaluate the activities of rifampicin, rifabutin and rifapentine in osteoblast infection models. Methods Using three S. aureus isolates, rifamycins were compared regarding: (i) their intracellular activity in ‘acute’

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Rudkin, Justine K., Maisem Laabei, Andrew M. Edwards, et al. "Oxacillin Alters the Toxin Expression Profile of Community-Associated Methicillin-Resistant Staphylococcus aureus." Antimicrobial Agents and Chemotherapy 58, no. 2 (2013): 1100–1107. http://dx.doi.org/10.1128/aac.01618-13.

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ABSTRACTThe emergence of community-associated methicillin-resistantStaphylococcus aureus(CA-MRSA) is a growing cause for concern. These strains are more virulent than health care-associated MRSA (HA-MRSA) due to higher levels of toxin expression. In a previous study, we showed that the high-level expression of PBP2a, the alternative penicillin binding protein encoded by themecAgene on type II staphylococcal cassette chromosomemec(SCCmec) elements, reduced toxicity by interfering with the Agr quorum sensing system. This was not seen in strains carrying the CA-MRSA-associated type IV SCCmeceleme

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Kang, Chang Kyung, Jeong Eun Cho, Yoon Jeong Choi, et al. "agrDysfunction Affects Staphylococcal Cassette ChromosomemecType-Dependent Clinical Outcomes in Methicillin-Resistant Staphylococcus aureus Bacteremia." Antimicrobial Agents and Chemotherapy 59, no. 6 (2015): 3125–32. http://dx.doi.org/10.1128/aac.04962-14.

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ABSTRACTStaphylococcal cassette chromosomemecelement (SCCmec) type-dependent clinical outcomes may vary due to geographical variation in the presence of virulence determinants. We compared the microbiological factors and mortality attributed to methicillin-resistantStaphylococcus aureus(MRSA) bacteremia between SCCmectypes II/III and type IV. All episodes of MRSA bacteremia in a tertiary-care hospital (South Korea) over a 4.5-year period were reviewed. We studied the microbiological factors associated with all blood MRSA isolates, includingspatype,agrtype,agrdysfunction, and the genes for Pant

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Chang, Spencer, Vance G. Fowler, Batu K. Sharma-Kuinkel, et al. "2594. Biofilm-Dispersed Staphylococcus aureus Exhibits a Distinct agr-Independent Host Interaction." Open Forum Infectious Diseases 6, Supplement_2 (2019): S901—S902. http://dx.doi.org/10.1093/ofid/ofz360.2272.

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Abstract Background Staphylococcus aureus biofilms are a common cause of persistent, life-threatening infections. Dispersal of S. aureus cells from established biofilm-based infections is crucial for dissemination within the host, but is poorly understood. We tested the hypothesis that biofilm dispersed S. aureus cells have distinct physiology from planktonic cells and are better equipped to evade host immunity in an agr-dependent manner. Methods Primary murine bone marrow-derived macrophages (BMDMs) were infected with planktonic and biofilm dispersed cells from S. aureus USA300 LAC wild type

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Hommes, Josefien W., Rachel M. Kratofil, Sigrid Wahlen, et al. "High density lipoproteins mediate in vivo protection against staphylococcal phenol-soluble modulins." Scientific Reports 11, no. 1 (2021). http://dx.doi.org/10.1038/s41598-021-94651-1.

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AbstractStaphylococcus aureus virulence has been associated with the production of phenol-soluble modulins (PSMs). These PSMs have distinct virulence functions and are known to activate, attract and lyse neutrophils. These PSM-associated biological functions are inhibited by lipoproteins in vitro. We set out to address whether lipoproteins neutralize staphylococcal PSM-associated virulence in experimental animal models. Serum from both LCAT an ABCA1 knockout mice strains which are characterised by near absence of high-density lipoprotein (HDL) levels, was shown to fail to protect against PSM-i

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Zaman, Masihuz, and Maria Andreasen. "Cross-talk between individual phenol-soluble modulins in Staphylococcus aureus biofilm enables rapid and efficient amyloid formation." eLife 9 (December 1, 2020). http://dx.doi.org/10.7554/elife.59776.

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The infective ability of the opportunistic pathogen Staphylococcus aureus, recognized as the most frequent cause of biofilm-associated infections, is associated with biofilm-mediated resistance to host immune response. Phenol-soluble modulins (PSM) comprise the structural scaffold of S. aureus biofilms through self-assembly into functional amyloids, but the role of individual PSMs during biofilm formation remains poorly understood and the molecular pathways of PSM self-assembly are yet to be identified. Here we demonstrate high degree of cooperation between individual PSMs during functional am

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Jiang, Qiu, Zeyu Jin, and Baolin Sun. "MgrA Negatively Regulates Biofilm Formation and Detachment by Repressing the Expression of psm Operons in Staphylococcus aureus." Applied and Environmental Microbiology 84, no. 16 (2018). http://dx.doi.org/10.1128/aem.01008-18.

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ABSTRACT Phenol-soluble modulins (PSMs) are amphipathic peptides that are produced by staphylococci and play important roles in Staphylococcus aureus biofilm formation and dissemination. Although the multiple functions of PSMs have been recognized, the regulatory mechanisms controlling the expression of psm operons remain largely unknown. In this study, we identified MgrA in a DNA pulldown assay and further demonstrated, by electrophoretic mobility shift assays and DNase I footprinting assays, that MgrA could bind specifically to the promoter regions of psm operons. We then constructed an isog

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Kawada-Matsuo, Miki, Atsuko Watanabe, Kaoru Arii, et al. "Staphylococcus aureus Virulence Affected by an Alternative Nisin A Resistance Mechanism." Applied and Environmental Microbiology 86, no. 8 (2020). http://dx.doi.org/10.1128/aem.02923-19.

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ABSTRACT Nisin A is a bacteriocin produced by Lactococcus lactis and is widely used as a food preservative. Staphylococcus aureus has the BraRS-VraDE system that provides resistance against low concentrations of nisin A. BraRS is a two-component system that induces the expression of the ABC transporter VraDE. Previously, we isolated a highly nisin A-resistant strain with increased VraDE expression due to a mutation in braRS. In this study, we isolated S. aureus MW2 mutants with BraRS-VraDE-independent nisin A resistance. These mutants, designated SAN2 (S. aureus nisin resistant) and SAN469, ha

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27

Schlatterer, Katja, Christian Beck, Dennis Hanzelmann, et al. "The Mechanism behind Bacterial Lipoprotein Release: Phenol-Soluble Modulins Mediate Toll-Like Receptor 2 Activation via Extracellular Vesicle Release from Staphylococcus aureus." mBio 9, no. 6 (2018). http://dx.doi.org/10.1128/mbio.01851-18.

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ABSTRACT The innate immune system uses Toll-like receptor (TLR) 2 to detect conserved bacterial lipoproteins of invading pathogens. The lipid anchor attaches lipoproteins to the cytoplasmic membrane and prevents their release from the bacterial cell envelope. How bacteria release lipoproteins and how these molecules reach TLR2 remain unknown. Staphylococcus aureus has been described to liberate membrane vesicles. The composition, mode of release, and relevance for microbe-host interaction of such membrane vesicles have remained ambiguous. We recently reported that S. aureus can release lipopro

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Shen, Tianwei, Kelly M. Hines, Nathaniel K. Ashford, Brian J. Werth, and Libin Xu. "Varied Contribution of Phospholipid Shedding From Membrane to Daptomycin Tolerance in Staphylococcus aureus." Frontiers in Molecular Biosciences 8 (June 11, 2021). http://dx.doi.org/10.3389/fmolb.2021.679949.

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It has been suggested that daptomycin can be inactivated by lipids released by Staphylococcus aureus and that this effect is antagonized by phenol soluble modulins (PSMs), which bind to the shed lipids. PSM production is regulated by the Agr system, and others have shown that loss of the Agr function enhances S. aureus survival in the presence of daptomycin. Here we assessed the impact of Agr function on daptomycin activity and lipid metabolism under various conditions. Daptomycin activity was evaluated against three sets of isogenic strain series with wild-type or dysfunctional Agr using stat

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Bloes, Dominik Alexander, Emanuel Haasbach, Carmen Hartmayer, et al. "Phenol-Soluble Modulin Peptides Contribute to Influenza A Virus-Associated Staphylococcus aureus Pneumonia." Infection and Immunity 85, no. 12 (2017). http://dx.doi.org/10.1128/iai.00620-17.

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ABSTRACT Influenza A virus (IAV) infection is often followed by secondary bacterial lung infection, which is a major reason for severe, often fatal pneumonia. Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) strains such as USA300 cause particularly severe and difficult-to-treat cases of IAV-associated pneumonia. CA-MRSA strains are known to produce extraordinarily large amounts of phenol-soluble modulin (PSM) peptides, which are important cytotoxins and proinflammatory molecules that contribute to several types of S. aureus infection. However, their potential role in

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Kretschmer, Dorothee, Ricarda Breitmeyer, Cordula Gekeler, et al. "Staphylococcus aureus Depends on Eap Proteins for Preventing Degradation of Its Phenol-Soluble Modulin Toxins by Neutrophil Serine Proteases." Frontiers in Immunology 12 (September 6, 2021). http://dx.doi.org/10.3389/fimmu.2021.701093.

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Neutrophil granulocytes act as a first line of defense against pathogenic staphylococci. However, Staphylococcus aureus has a remarkable capacity to survive neutrophil killing, which distinguishes it from the less-pathogenic Staphylococcus epidermidis. Both species release phenol-soluble modulin (PSM) toxins, which activate the neutrophil formyl-peptide receptor 2 (FPR2) to promote neutrophil influx and phagocytosis, and which disrupt neutrophils or their phagosomal membranes at high concentrations. We show here that the neutrophil serine proteases (NSPs) neutrophil elastase, cathepsin G and p

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Knott, Samantha, Dylan Curry, Neil Zhao, et al. "Staphylococcus aureus Floating Biofilm Formation and Phenotype in Synovial Fluid Depends on Albumin, Fibrinogen, and Hyaluronic Acid." Frontiers in Microbiology 12 (April 29, 2021). http://dx.doi.org/10.3389/fmicb.2021.655873.

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Biofilms are typically studied in bacterial media that allow the study of important properties such as bacterial growth. However, the results obtained in such media cannot take into account the bacterial localization/clustering caused by bacteria–protein interactions in vivo and the accompanying alterations in phenotype, virulence factor production, and ultimately antibiotic tolerance. We and others have reported that methicillin-resistant or methicillin-susceptible Staphylococcus aureus (MRSA or MSSA, respectively) and other pathogens assemble a proteinaceous matrix in synovial fluid. This pr

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Joo, Hwang-Soo, Som S. Chatterjee, Amer E. Villaruz, et al. "Mechanism of Gene Regulation by a Staphylococcus aureus Toxin." mBio 7, no. 5 (2016). http://dx.doi.org/10.1128/mbio.01579-16.

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ABSTRACT The virulence of many bacterial pathogens, including the important human pathogen Staphylococcus aureus , depends on the secretion of frequently large amounts of toxins. Toxin production involves the need for the bacteria to make physiological adjustments for energy conservation. While toxins are primarily targets of gene regulation, such changes may be accomplished by regulatory functions of the toxins themselves. However, mechanisms by which toxins regulate gene expression have remained poorly understood. We show here that the staphylococcal phenol-soluble modulin (PSM) toxins have

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