The enemy within

By Philip Cohen BY STIFLING part of a rat’s immune system, researchers in Michigan have been able to protect the animal from sepsis. In such life-threatening bacterial infections, toxins released into the blood can cause organ failure or trigger severe inflammation and fatal tissue damage. Even after antibiotic treatment, more than 20 per cent of patients die from the condition. One of the immune system’s ways of fighting bacteria is with a collection of more than a dozen proteins known as complement. Complement doesn’t have to learn to recognise invaders as antibodies do. Instead, it gets to work immediately, rallying immune cells and chemical weapons to destroy the microbes. So immunologist Peter Ward of the University of Michigan Medical School in Ann Arbor and his team were reasonably sure that removing any key player in the complement would only give sepsis the upper hand. To test that theory, they induced sepsis in rats and immediately removed two complement proteins from their blood. More than 90 per cent of the animals that received no treatment were dead after a week. And as expected, animals that had lost complement protein C3 died even faster. All had succumbed by the fifth day. But, to Ward’s surprise, rats without their C5 protein actually fared better. Fifty per cent survived for at least ten days. According to Ward, “This protection was astounding to us.” Complement protein C5 normally helps immune cells called neutrophils to produce hydrogen peroxide, which helps to destroy bacteria. But it turned out that in the rats the antibody that was supposed to knock out all of C5 had instead only attacked one fragment, C5a. Removing this fragment actually seemed to help the sick rats. The researchers discovered that untreated animals’ neutrophils were producing about 60 per cent less hydrogen peroxide than animals treated with the antibody to C5a, they report in Nature Medicine (vol 5, p 788). While C5a usually activates neutrophils, Ward believes that so much of the protein is produced during sepsis that it “burns out” the neutrophils, blunting their ability to fight infection. So reducing C5a levels actually helps keep the neutrophils fighting fit. “It’s an enticing model to explain how sepsis works,” says Alfred Ayala, an immunologist at Brown University School of Medicine in Rhode Island. In fact,
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