Food poisoning may cause more trouble than a few days' nausea--a toxin released by at least one sickening bacteria also scrambles the DNA of cells it infects. The newly found mechanism is probably shared by many pathogenic bacteria, researchers suspect, and it could explain why bacterial infections increase the risk of cancer.
Campylobacter pylori causes more cases of food poisoning in the United States than any other microbe. The bug, which thrives in raw meat, produces a toxin called CDT. If Campylobacter is ingested, the toxin infects cells in the intestines, causing the cells to stop dividing and swell up. Whether this talent benefits Campylobacter has been unclear: It may somehow create a more comfortable environment for the bug, or it may thwart the host's immune system. Also unknown has been how the toxin works.
Hunting for an answer, microbiologists Maria Lara-Tejero and Jorge Galán of Yale University School of Medicine focused on the three genes responsible for making the toxin. They wanted to know which one held the power to stop cell division, or "arrest" the cell. By inserting each gene separately into mammalian cells, they found their target: the gene that produces a protein called CdtB. The sequence of that gene, the researchers found, resembles a family of proteins called DNases, which chew up DNA. The researchers think that CdtB chops up its host DNA just enough to call the host's damage surveillance machinery into action--thereby arresting the cell but not killing it, the researchers report in the 13 October issue of Science.
While most toxins wreak havoc by modifying or destroying host proteins, going after host DNA may not be unusual. In fact, a research team from the University of Missouri, Kansas City, reported in the August issue of Molecular Microbiology that the CdtB from another bacterium, Eschericia coli, could chop up DNA in a test tube and cause cultured cells to stop dividing.
Inflicting DNA damage is "a neat explanation for how arrest occurs," says John Leong of the University of Massachusetts Medical Center in Worcester. CdtB could cause mutations that increase the risk of intestinal cancer, says David Schauer of the Massachusetts Institute of Technology, although he points out that inflammation from an infection could do more damage to DNA than the toxin itself.