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Article Abstract
Two large-scale outbreaks of streptococcal toxic shock-like syndrome (STSLS) have revealed 2 to be a severe and evolving human pathogen. We investigated the mechanism by which 2 causes STSLS. The transcript abundance of the transcriptional regulator gene was found to be upregulated during experimental infection. Compared with the wild-type 05ZY strain, a deletion mutant (Δ) elicited reduced cytokine secretion in macrophages. In a murine infection model, deletion resulted in decreased virulence and bacterial load, and affected cytokine production. Moreover, TstS expression in the P1/7 strain of led to the induction of STSLS in the infected mice. This is noteworthy because, although it is virulent, the P1/7 strain does not normally induce STSLS. Through a microarray-based comparative transcriptomics analysis, we found that TstS regulates multiple metabolism-related genes and several virulence-related genes associated with immune evasion.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6020791 | PMC |
| http://dx.doi.org/10.3389/fmicb.2018.01309 | DOI Listing |
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