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Staphylococcal Skin Infections01:29

Staphylococcal Skin Infections

Staphylococcus aureus is a Gram-positive coccus that resides harmlessly on the skin and mucous membranes of healthy individuals. When the skin barrier is breached, it can shift from a commensal to an opportunistic pathogen. This transition is facilitated by surface adhesins, such as clumping factor B and S. aureus surface protein G (SasG), which bind to structural proteins, including loricrin and cytokeratin, in the damaged epidermis. Protein A, another key factor, binds the Fc region of...
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Biofilms are complex communities of microorganisms encased in a self-produced extracellular polysaccharide matrix attached to surfaces. These microbial consortia can include single or multiple species, providing enhanced survival benefits by forming organized, multilayered structures.The formation of biofilms occurs through four key stages: attachment, colonization, development, and dispersal.During attachment, free-swimming planktonic cells adhere to a surface, often facilitated by...
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Quorum sensing is a mechanism of bacterial communication that enables coordinated gene expression in response to changes in population density. This facilitates collective behaviors that enhance survival, resource acquisition, and ecological adaptation. This process relies on small signaling molecules called autoinducers that accumulate as bacterial populations grow. When a critical threshold concentration of autoinducers is reached, bacterial cells collectively modify gene expression,...
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Methicillin-resistant Staphylococcus aureus (MRSA) presents a critical public health threat, arising from its capacity to resist β-lactam antibiotics due to acquisition of the mecA gene within the staphylococcal cassette chromosome mec (SCCmec). This gene encodes penicillin-binding protein 2a (PBP2a), which impairs binding efficacy of methicillin and other β-lactams. MRSA has evolved into distinct clonal lineages impacting humans and animals alike, reinforcing its significance within the One...
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A Platform of Anti-biofilm Assays Suited to the Exploration of Natural Compound Libraries
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Published on: December 27, 2016

Staphopains modulate Staphylococcus aureus biofilm integrity.

Joe M Mootz1, Cheryl L Malone, Lindsey N Shaw

  • 1Department of Microbiology, Roy J and Lucille A Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA.

Infection and Immunity
|June 27, 2013
PubMed
Summary

Staphylococcus aureus cysteine proteases SspB and ScpA (Staphopains) are key to biofilm structure. Inhibiting or deleting these proteases prevents and disperses S. aureus biofilms, offering new therapeutic targets.

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Standardized In vitro Assays to Visualize and Quantify Interactions between Human Neutrophils and Staphylococcus aureus Biofilms

Published on: June 8, 2022

Area of Science:

  • Microbiology
  • Molecular Biology
  • Biochemistry

Background:

  • Staphylococcus aureus forms chronic biofilm infections on medical devices and host tissues.
  • Proteinaceous material is crucial for biofilm structure, with secreted proteases potentially altering biofilm integrity.
  • The precise role of individual proteases in S. aureus biofilm modulation remains unclear.

Purpose of the Study:

  • To identify specific proteases involved in Staphylococcus aureus biofilm formation and architecture.
  • To elucidate the mechanism by which proteases influence biofilm integrity.
  • To investigate the potential of targeting these proteases for antibiofilm strategies.

Main Methods:

  • Utilized a sigma factor B (ΔsigB) mutant strain exhibiting a biofilm-negative phenotype to identify key proteases.
  • Employed plasma-coated microtiter assays and flow cell biofilms to assess biofilm formation.
  • Used protease inhibitors (E-64, Staphostatins) and constructed gene deletion mutants (sspB, scpA) to evaluate protease function.
  • Administered purified SspB and ScpA enzymes to S. aureus biofilms.

Main Results:

  • Biofilm formation was restored in the ΔsigB mutant by inhibiting cysteine proteases SspB and ScpA (Staphopains).
  • A double mutant lacking both sspB and scpA genes restored biofilm formation in the ΔsigB background.
  • Extracellular Staphopain levels decreased during biofilm formation, potentially facilitating biofilm establishment.
  • Purified SspB and ScpA inhibited biofilm formation, with ScpA also dispersing established biofilms across various strains.

Conclusions:

  • The extracellular cysteine proteases SspB and ScpA play a significant, underappreciated role in modulating Staphylococcus aureus biofilm architecture.
  • Targeting SspB and ScpA offers a promising strategy for combating chronic S. aureus biofilm infections.
  • Understanding protease activity is crucial for developing effective antibiofilm therapies against S. aureus.