Proinflammatory exoprotein characterization of toxic shock syndrome staphylococcus aureus

Ying Chi Lin, Michele J. Anderson, Petra L. Kohler, Kristi L. Strandberg, Michael E. Olson, Alexander R. Horswill, Patrick M. Schlievert, Marnie L. Peterson

Research output: Contribution to journalArticlepeer-review

25 Scopus citations

Abstract

Pulsed-field gel electrophoresis (PFGE) clonal type USA200 is the most widely disseminated Staphylococcus aureus colonizer of the nose and is a major cause of toxic shock syndrome (TSS). Exoproteins derived from these organisms have been suggested to contribute to their colonization and causation of human diseases but have not been well-characterized. Two representative S. aureus USA200 isolates, MNPE (δ-toxin positive) and CDC587 (δ-toxin mutant), isolated from pulmonary post-influenza TSS and menstrual vaginal TSS, respectively, were evaluated. Biochemical, immunobiological, and cell-based assays, including mass spectrometry, were used to identify key exoproteins derived from the strains that are responsible for proinflammatory and cytotoxic activity on human vaginal epithelial cells. Exoproteins associated with virulence were produced by both strains, and cytolysins (δ-toxin and -toxin), superantigens, and proteases were identified as the major exoproteins, which caused epithelial cell inflammation and cytotoxicity. Exoprotein fractions from MNPE were more proinflammatory and cytotoxic than those from CDC587 due to high concentrations of δ-toxin. CDC587 produced a small amount of δ-toxin, despite the presence of a stop codon (TAG) at codon 113. Additional exotoxin identification studies of USA200 strain [S. aureus MN8 (δ-toxin mutant)] confirmed that MN8 also produced low levels of δ-toxin despite the same stop codon. The differences observed in virulence factor profiles of two USA200 strains provide insight into environmental factors that select for specific virulence factors. Cytolysins, superantigens, and proteases were identified as potential targets, where toxin neutralization may prevent or diminish epithelial damage associated with S. aureus.

Original languageEnglish (US)
Pages (from-to)7157-7167
Number of pages11
JournalBiochemistry
Volume50
Issue number33
DOIs
StatePublished - Aug 23 2011

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