Putting the brakes on toxic shock

Scientists in Sweden have discovered the cascade of molecular events that underpins many cases of toxic shock syndrome. The researchers have even successfully foiled this deadly sequence in animals, suggesting that a similar approach might benefit people.

Some cases of toxic shock syndrome arise from streptococcus infections. In these, a bacterial protein called M protein incites massive leakage from blood vessels. Blood pressure plummets, throwing the body into shock, while blood-starved organs fail. Fatality rates range from 30 percent to 70 percent.

Past research has revealed that M protein binds to the blood protein fibrinogen. In the Feb. 6 Cell, molecular biologist Heiko Herwald of Lund University and his colleagues spell out a complex reaction whereby this protein duplex binds to immune cells called neutrophils. This stimulates the neutrophils to produce yet another protein, heparin-binding protein, which causes the blood leakage, says Herwald.

The Swedish researchers tested a compound that previous research suggested could inhibit neutrophil-fibrinogen binding. In test tubes, this short-circuited the molecular cascade. Since damage from the syndrome often shows up in the lungs, the researchers looked in mouse lungs for proof of the biochemical short circuit. Indeed, they found little lung damage in animals getting M protein plus the inhibitor but severe damage in other mice given M protein but no inhibitor.

Only further studies will ascertain whether this approach could prove safe in people, Herwald says.

A strategy targeting M protein wouldn’t apply to cases of toxic shock syndrome caused by staphylococcus infections.

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