Experts discover how anthrax toxins disrupt cell mechanisms

Two groups of anthrax experts at the University of California San Diego recently discovered how two separate toxins from anthrax bacteria function to disrupt critical cell mechanisms during infection.

One group examined anthrax in mice and human cells, while the other looked at how the deadly bioterrorism agent functioned in fruit flies. Together, they showed that the toxins worked in conjunction to stop the final step in a process that allows cells to communicate and adhere to one another through the transportation of certain molecules, according to

The UCSD researchers' report, published in the October 14 issue of the journal Nature, concludes that by interfering with the sites of cell to cell communication, anthrax stops the flow of molecular components critical to cell functioning, leading to the failure of critical blood vessels. During the final stages of infection, this is what usually kills victims.

“We know that one key reason that anthrax kills is by making blood vessels and cell barriers leaky,” Ethan Bier, a UCSD biology professor and senior author of the paper, told “But the mystery has been how these dangerous changes could be related to two very different types of toxins the bacteria inject into their hosts?”

The first major clue to this mystery appeared when two scientists from the first group of researchers noticed that the anthrax toxins worked together to produce unusual notches in the wings of fruit flies.

“By impinging on two pivotal regulators of the cellular mail service, these two toxins effectively eliminated the delivery of critical components to zones essential for cells communicating with each other and forming coherent structures such as the wing margins of flies,” Bier said, reports.

The other group of researchers followed up by finding that human cells treated with anthrax toxins had similar defects. They also found that injecting live anthrax bacteria into the lungs or under the skin of mice could cause nearby blood vessels to leak, whereas mutant strains of anthrax bacteria that did not contain the two toxins had no such effect.

“Our studies with human cells and mice suggest that the ability of anthrax toxins to inhibit delivery of adhesive molecules to sites responsible for cell to cell contact leads to leaky blood vessels and may contribute to the final stages of anthrax infection in which blood vessels fail and the patient develops shock, often followed by rapid death,” Victor Nizet, the head of the second research team, told

The information the two teams found during their study is becoming increasingly important as scientist try to find better ways to protect large numbers of people from bioterrorist threats.