Related Experiment Video

Updated: May 28, 2026

Biomimetic Materials to Characterize Bacteria-host Interactions
12:22

Biomimetic Materials to Characterize Bacteria-host Interactions

Published on: November 16, 2015

A new anti-infective strategy to reduce adhesion-mediated virulence in Staphylococcus aureus affecting surface

M Artini1, G L Scoarughi, R Papa

  • 1Department of Public Health and Infectious Diseases, Sapienza University, Rome, Italy.

International Journal of Immunopathology and Pharmacology
|October 8, 2011
PubMed

Insights

Serratiopeptidase (SPEP) can combat Staphylococcus aureus infections by disrupting bacterial adhesion and biofilm formation. This enzyme shows potential as an anti-infective agent against medical device-related infections.

Area of Science:

  • Microbiology
  • Biochemistry
  • Infectious Diseases

Background:

  • Staphylococcus aureus is a major cause of community and hospital-acquired infections, often linked to medical devices.
  • This pathogen utilizes virulence factors like toxins, cell invasion, and biofilm formation to cause infection.
  • Indwelling medical devices significantly increase the risk of Staphylococcus aureus infections.

Purpose of the Study:

  • To evaluate the anti-infective properties of serratiopeptidase (SPEP) against Staphylococcus aureus.
  • To investigate SPEP's ability to impair staphylococcal virulence factors, including surface attachment, adhesion, and invasion.
  • To identify the specific staphylococcal proteins affected by SPEP treatment.

Main Methods:

  • Proteomic analysis of surface proteins from SPEP-treated Staphylococcus aureus cultures.
  • Evaluation of SPEP's effect on bacterial attachment to inert surfaces.
  • Assessment of SPEP's impact on bacterial adhesion and invasion of eukaryotic cells.

Main Results:

  • SPEP treatment affected several key staphylococcal surface proteins, including adhesin/autolysin Atl, FnBP-A, SecA1, Sbi, EF-Tu, EF-G, and alpha-enolase.
  • SPEP demonstrated the ability to impair Staphylococcus aureus attachment to inert surfaces.
  • The study indicated that SPEP hinders bacterial adhesion and invasion of eukaryotic cells.

Conclusions:

  • Serratiopeptidase (SPEP) exhibits anti-infective properties against Staphylococcus aureus.
  • SPEP may hinder Staphylococcus aureus entry into host tissues and reduce biofilm formation on medical devices.
  • SPEP holds potential as a therapeutic agent to combat Staphylococcus aureus infections, particularly those associated with medical devices.

More Related Videos

Improved Enzyme Protection Assay to Study Staphylococcus aureus Internalization and Intracellular Efficacy of Antimicrobial Compounds06:36

Improved Enzyme Protection Assay to Study Staphylococcus aureus Internalization and Intracellular Efficacy of Antimicrobial Compounds

Published on: September 8, 2021

A Platform of Anti-biofilm Assays Suited to the Exploration of Natural Compound Libraries09:39

A Platform of Anti-biofilm Assays Suited to the Exploration of Natural Compound Libraries

Published on: December 27, 2016

Related Concept Videos

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...
Clinical Significance of Antibiotic Resistance01:25

Clinical Significance of Antibiotic Resistance

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...
Determinants of Bacterial Pathogenicity and Virulence01:20

Determinants of Bacterial Pathogenicity and Virulence

Pathogenic bacteria employ a variety of strategies to establish infections, including the secretion of extracellular enzymes that act as potent virulence factors. These enzymes facilitate bacterial colonization of host tissues and help evade immune surveillance. By targeting structural components of host tissues and interfering with immune mechanisms, these enzymes play a pivotal role in disease progression.Extracellular Enzymes Facilitating Tissue Invasion: Several bacterial pathogens secrete...
Mechanism of Antibiotic Resistance in MRSA01:25

Mechanism of Antibiotic Resistance in MRSA

Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and acquisition...
Surface Membrane Barriers01:18

Surface Membrane Barriers

The skin and mucous membranes serve as the primary line of defense against pathogens by providing both physical and chemical protection. These barriers are essential in preventing the entry and establishment of microbes, thereby maintaining the integrity of the host.
The outer layer of the skin, the epidermis, is a robust barrier comprising layers of closely packed keratinized cells. This dense arrangement prevents microbes from penetrating the body. The periodic shedding of epidermal cells...
Gene Regulation in Microbial Communities: Quorum Sensing01:28

Gene Regulation in Microbial Communities: Quorum Sensing

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,...