Leading the Way in Life Science Technologies

GEN Exclusives

More »

GEN News Highlights

More »
Aug 29, 2013

How Anthrax Kills

  • NIH scientists say they have identified the cells in two different areas of the body that are specifically targeted by anthrax toxins. The researchers published their study (“Key tissue targets responsible for anthrax-toxin-induced lethality”) in this week’s issue of Nature.

    Bacillus anthracis produces two deadly toxins: lethal toxin and edema toxin. When B. anthracis infects a human or animal, both toxins seek out and bind to receptors on the surfaces of human and animal cells. Using two types of laboratory mice—those missing the anthrax toxin receptor on a single type of cell or those having the receptor present on a single type of cell—the scientists compared disease progression among the rodents. The investigators, from the National Institute of Allergy and Infectious Diseases and the National Heart, Lung, and Blood Institute, concluded that anthrax-induced death is caused primarily by lethal toxin targeting heart cells and muscle cells surrounding blood vessels, and edema toxin targeting liver cells.

    The scientists believe the results of their animal studies can prove useful to people afflicted with the disease.

    “The findings reported here may have value in understanding the pathogenesis of human anthrax infections,” they wrote in the journal paper. “Recognition that the anthrax toxins are targeting the cardiovascular system and liver may suggest specific supportive therapies that would limit tissue damage and increase survival. Re-examination of the clinical course, pathology, and autopsy reports of the relatively few well-documented human anthrax cases in light of the data presented here may provide additional insights.”

Related content

Be sure to take the GEN Poll

CRISPR Patent Controversy

Do you think recently released email from a former Broad Institute scientist to Jennifer Doudna will expedite a final legal decision on who owns the CRISPR patent?

More »