A drug composed of an ordinary antibiotic combined with a microbe-fighting compound may be enough to protect thousands of people from the ravages of radiation sickness in the aftermath of a major nuclear accident or attack, experiments with mice suggest.
Researchers exposed mice to a heavy dose of radiation and 24 hours later gave some of them injections of an antibiotic and a protein that’s made naturally by the immune system. Thirty days later, most mice that received no treatment were dead, whereas nearly 80 percent of mice that received the treatment still appeared healthy, a team reports in the Nov. 23 Science Translational Medicine.
Follow-up studies are still needed before the combo can be used to treat people, but versions of the antibiotic and the protein have already been used in humans, so the new approach looks promising. It might even be used as a preemptive measure for first responders.
“This could potentially be very useful,” says radiobiologist Gayle Woloschak of Northwestern University in Chicago, who was not involved with the study.
Radiation exposure of levels up to 10 gray (the mice received 7 gray, about 45,000 times the dose of a chest X-ray) would usually require a bone marrow transplant and probably treatment with a compound that stimulates bone marrow growth. “During a mass casualty event you’re not going to be able to do bone marrow transplants,” says Woloschak. And while questions remain about long-term survival of mice given the new treatment, “it’s quite exciting,” she says.
When the body is exposed to intense levels of radiation, bone marrow is one of the first things to shut down. Bone marrow is where most white blood cells arise, so the body’s immune system can’t fight infection properly when compromised. And a working, fighting immune system is just what’s needed after exposure to radiation. Radiation can cause bacteria that are usually confined to the gut to leak into the blood, causing blood pressure to spike, fever, abnormal blood clotting and even organ failure.
The new treatment goes after these marauding bacteria. The fluoroquinolone antibiotic, a mouse version of Cipro, aims to kill any bacteria it comes across. And the protein, called BPI, mops up and latches onto bacterial endotoxin, a nasty molecule on the coats of many bacteria.
“We think we have a combination here that is multifunctional,” says stem cell transplant doctor Eva Guinan of the Dana-Farber Cancer Institute and Harvard Medical School, who led the work with Ofer Levy, also of Harvard and Children’s Hospital Boston. “We still have a lot more to explore in detail, but the results are really encouraging.”
