Putting the brakes on toxic shock.Scientists in Sweden have discovered the cascade of molecular events that underpins many cases of toxic shock syndrome toxic shock syndrome (TSS). acute, sometimes fatal, disease characterized by high fever, nausea, diarrhea, lethargy, blotchy rash, and sudden drop in blood pressure. It is caused by Staphylococcus aureus, an exotoxin-producing bacteria (see toxin). . 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 streptococcus (strĕp'təkŏk`əs), any of a group of gram-positive bacteria, genus Streptococcus, some of which cause disease. infections. In these, a bacterial protein called M protein incites massive leakage from blood vessels Blood vessels Tubular channels for blood transport, of which there are three principal types: arteries, capillaries, and veins. Only the larger arteries and veins in the body bear distinct names. . 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 Fibrinogen The major clot-forming substrate in the blood plasma of vertebrates. Though fibrinogen represents a small fraction of plasma proteins (normal human plasma has a fibrinogen content of 2–4 mg/ml of a total of 70 mg protein/ml), its conversion . 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 neutrophils (ner·ō·trōˑ·filz), n.pl white blood cells with cytoplasmic granules that consume harmful bacteria, fungi, and other foreign materials. . 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 staphylococcus (stăf'ələkŏk`əs), any of the pathogenic bacteria, parasitic to humans, that belong to the genus Staphylococcus. The spherical bacterial cells (cocci) typically occur in irregular clusters [Gr. infections.--N.S. |
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