Phenol-soluble modulins--critical determinants of staphylococcal virulence

Gordon Y C Cheung1, Hwang-Soo Joo, Som S Chatterjee

  • 1Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, The National Institutes of Health, Bethesda, MD, USA.

FEMS Microbiology Reviews
|December 31, 2013
PubMed

Insights

Phenol-soluble modulin (PSM) peptides are crucial for staphylococcal infections, aiding in virulence and biofilm formation. Targeting these peptides offers a promising strategy for developing new anti-staphylococcal drugs.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Biochemistry

Background:

  • Phenol-soluble modulins (PSMs) are amphipathic, alpha-helical peptides produced by staphylococci.
  • PSMs play significant roles in staphylococcal pathogenesis, including cytolysis and biofilm development.

Purpose of the Study:

  • To review the biochemistry, genetics, and roles of PSMs in staphylococcal commensal and pathogenic lifestyles.
  • To discuss how PSM diversification influences staphylococcal species aggressiveness.
  • To evaluate PSMs as potential drug targets for treating staphylococcal infections.

Main Methods:

  • Literature review of existing research on PSMs.
  • Analysis of biochemical and genetic data related to PSMs.
  • Evaluation of PSM functions in various staphylococcal lifestyles.

Main Results:

  • PSMs contribute to the pathogenic success of virulent staphylococci like Staphylococcus aureus.
  • PSMs can lyse human cells (leukocytes, erythrocytes) and stimulate inflammatory responses.
  • Diversification of PSMs correlates with the aggressiveness of different staphylococcal species.

Conclusions:

  • PSMs have evolved from facilitating commensal growth to driving aggressive pathogenesis in virulent strains.
  • Targeting PSMs presents a viable therapeutic strategy against staphylococcal infections.

Related Concept Videos

Regulation of Bacterial Virulence01:28

Regulation of Bacterial Virulence

Pathogenic bacteria employ a range of regulatory mechanisms to modulate the expression of virulence genes in response to environmental and host-derived signals. These mechanisms ensure that virulence factors are expressed only under favorable conditions, thereby optimizing infection and survival strategies.Mechanisms of Virulence RegulationKey regulatory strategies include:Two-Component Systems: These consist of a membrane-bound sensor kinase and a cytoplasmic response regulator. Environmental...
76
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,...
954
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...
90
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...
219
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
24
Bacterial Toxins01:12

Bacterial Toxins

Bacterial toxins are sophisticated virulence factors that enable pathogenic bacteria to interact with, invade, and damage host tissues. These toxins fall broadly into two types: protein exotoxins, which are secreted into the environment and target specific host receptors, and lipopolysaccharide endotoxins, which are structural components of the bacterial outer membrane released primarily during bacterial lysis or membrane shedding. Exotoxins generally act more selectively, binding to cell...
148