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Review
. 2018 Jun 19;10(6):252.
doi: 10.3390/toxins10060252.

Staphylococcus aureus Toxins and Their Molecular Activity in Infectious Diseases

Diana Oliveira  1 , Anabela Borges  2 , Manuel Simões  3
Affiliations
Review

Staphylococcus aureus Toxins and Their Molecular Activity in Infectious Diseases

Diana Oliveira et al. Toxins (Basel). .

Abstract

Staphylococcus aureus is a microorganism resident in the skin and nasal membranes with a dreadful pathogenic potential to cause a variety of community and hospital-acquired infections. The frequency of these infections is increasing and their treatment is becoming more difficult. The ability of S. aureus to form biofilms and the emergence of multidrug-resistant strains are the main reasons determining the challenge in dealing with these infections. S. aureus' infectious capacity and its success as a pathogen is related to the expression of virulence factors, among which the production of a wide variety of toxins is highlighted. For this reason, a better understanding of S. aureus toxins is needed to enable the development of new strategies to reduce their production and consequently improve therapeutic approaches. This review focuses on understanding the toxin-based pathogenesis of S. aureus and their role on infectious diseases.

Keywords: Staphylococcus aureus; biofilms; epidemiology; exfoliative toxins; pore-forming toxins; superantigens.

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Conflict of interest statement

The authors declare no conflict of interest. The founding sponsors had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, and in the decision to publish the results.

Figures

Figure 1
Figure 1
Mechanism of action of Hemolysin-α (Hla). Hla is secreted as a water-soluble monomer (1). Hla binds to the transmembrane protein ADAM10 which is a cellular receptor for α-toxin (2). Then, the toxin oligomerizes into a heptamer on the plasma membrane and a pre-pore is formed (3) and, at the end, the formation of the transmembrane channel occurs (4).
Figure 2
Figure 2
Mechanism of action of leukotoxins. The monomers are secreted (1). The S-component binds the cell surface receptor (2) then, the F component is recruited, and dimerization occurs (3). These dimers oligomerize on the plasma membrane and a pre-pore appears (4). At last, the formation of the transmembrane channel occurs (5).
Figure 3
Figure 3
Model of pore-formation mechanism for S. aureus PSMs. PSMs attach the cytoplasmic membrane in a non-specific fashion (1), this can lead to membrane disintegration (2). PSMs have the tendency to aggregate in oligomers and form a pore, which is short-lived (3).
Figure 4
Figure 4
Proposed model for bacterial invasion and blistering provoked by staphylococcal ETs.
Figure 5
Figure 5
Mechanism of action of SAgs. SAg bind to MHC class II molecules and to a variable region of T-cell receptor, which leads to the stimulation of many T-cells.
See this image and copyright information in PMC

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