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Bacteria that release a toxin that forms a pore in red blood cells leading to hemolysis are using an alpha toxin to gain access to the nutrients inside the erythrocyte.
The best characterized and most potent membrane-damaging toxin of Staphylococcus aureus is α-toxin. It is expressed as a monomer that binds to the membrane of susceptible cells.
In humans, platelets and monocytes are specifically sensitive to α-toxin. They bear high affinity sites which allow the toxin to bind at concentrations that are physiologically relevant. A complex series of secondary reactions follow, leading to the release of eicosanoids and cytokines which in turn trigger the production of inflammatory mediators. These events cause the symptoms of septic shock that occur during severe infections caused by S. aureus.
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