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Thrombocytopenia or platelet dysfunction is a risk factor for severe infection.  Staphylococcus aureus  ( S. aureus ) releases a variety of virulence factors especially toxic shock syndrome toxin 1 (TSST-1), which may cause toxic shock syndrome.  S. aureus , when carrying the  tst  gene, is more prone to cause toxic shock syndrome and is responsible for an especially high rate of mortality. However, the effect of TSST-1 protein on platelets is unknown. Patients with the  tst  gene positive  S. aureus  bacteremia showed more serious infection, higher mortality and lower platelet count. The  tst  gene positive  S. aureus  strains induce more platelet apoptosis and activation and corresponding up-regulation of Bak and down-regulation of Bcl-XL in addition to the activation of Caspase-3. C57BL/6 mice infected with the  tst  gene positive strains resulted in both a decrease in platelet count and an increase in platelet apoptosis and/or activation events and mortality. Moreover, TSST-1 protein, encoded by  tst  gene, caused the decrease of platelet count, the increase of platelet apoptosis and activation events and the level of inflammatory cytokines  in vivo . However, TSST-1 protein was unable to induce traditional activation and apoptosis on human platelets  in vitro . These results suggested that TSST-1 protein may exert indirect effects on platelet activation and apoptosis  in vivo .

TSST-1 protein exerts indirect effect on platelet activation and apoptosis