Related Experiment Video

Updated: Mar 28, 2026

A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues
07:10

A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues

Published on: February 19, 2019

9.6K

Functional characteristics of the Staphylococcus aureus δ-toxin allelic variant G10S

Gordon Y C Cheung1, Anthony J Yeh1, Dorothee Kretschmer2

  • 1Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, The National Institutes of Health, Bethesda, MD 20892, United States of America.

Scientific Reports
|December 15, 2015
PubMed

Insights

The Staphylococcus aureus δ-toxin variant G10S has reduced cytolytic and inflammatory functions. However, this variant did not alter disease severity in mouse models, suggesting other phenol-soluble modulins (PSMs) may compensate in vivo.

Area of Science:

  • Microbiology
  • Immunology
  • Molecular Biology

Background:

  • Staphylococcus aureus phenol-soluble modulins (PSMs) are key virulence factors involved in cell lysis and inflammation.
  • δ-toxin, a member of the PSM family, is highly expressed but possesses moderate cytolytic activity.
  • An allelic variant, δ-toxin G10S, is prevalent in specific S. aureus lineages, including those causing community-associated infections.

Purpose of the Study:

  • To investigate the functional impact of the δ-toxin G10S allelic variant on S. aureus pathogenesis.
  • To compare the cytolytic and pro-inflammatory capacities of δ-toxin G10S with the wild-type variant.
  • To evaluate the in vivo relevance of δ-toxin G10S variation in a murine infection model.

Main Methods:

  • Comparative analysis of δ-toxin G10S and wild-type variants.
  • Assessment of cytolytic activity against red and white blood cells.
  • Measurement of pro-inflammatory cytokine induction.
  • Evaluation of disease severity in murine infection models using isogenic S. aureus strains.

Main Results:

  • δ-toxin G10S exhibited significantly reduced cytolytic and pro-inflammatory capacities compared to the wild-type.
  • These reductions were observed even in strain backgrounds with high production of other PSMs.
  • Isogenic strains expressing either δ-toxin variant did not result in measurable differences in disease severity in murine models.

Conclusions:

  • The G10S allelic variation in δ-toxin significantly impacts its intrinsic virulence functions.
  • The in vivo relevance of this variation may be masked by the potent activities of other PSMs in S. aureus.
  • This finding highlights the complex interplay of virulence factors in staphylococcal pathogenesis.

More Related Videos

A Tandem Liquid Chromatography–Mass Spectrometry-based Approach for Metabolite Analysis of Staphylococcus aureus08:03

A Tandem Liquid Chromatography–Mass Spectrometry-based Approach for Metabolite Analysis of Staphylococcus aureus

Published on: March 28, 2017

10.7K
Genome-wide Gene Deletions in Streptococcus sanguinis by High Throughput PCR14:07

Genome-wide Gene Deletions in Streptococcus sanguinis by High Throughput PCR

Published on: November 23, 2012

17.1K

Related Concept Videos

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...
34
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...
46
Bacterial Gastroenteritis01:18

Bacterial Gastroenteritis

Bacterial gastroenteritis, characterized by diarrhea, abdominal cramps, and vomiting, is often caused by ingestion of contaminated food or water and is frequently associated with pathogenic Escherichia coli strains. These microbes exploit two principal mechanisms to inflict disease.Shiga toxin–producing E. coli, also referred to as STEC—notably O157:H7—release Shiga toxins that target ribosomes, blocking protein synthesis. The B subunit of the toxin binds the host glycolipid...
32
Diphtheria01:28

Diphtheria

Diphtheria is an acute, toxin-mediated infectious disease that primarily affects the upper respiratory tract. It is caused by Corynebacterium diphtheriae, a Gram-positive, pleomorphic rod that lacks spore-forming capability and exhibits a characteristic club-shaped morphology under microscopic examination. While C. diphtheriae can asymptomatically colonize mucosal surfaces, clinical disease manifests only when the bacterial strain is lysogenized by a specific β-corynephage. This phage...
49
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...
26
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...
95