Researchers at the University of Chicago have discovered how Staphylococcus aureus, a common cause of life-threatening infections, manages to acquire iron from its host's red blood cells, a critical step in causing disease. The discovery, published in the 7 February 2003 issue of the journal Science, suggests new ways to combat this common pathogen, which has grown ominously resistant to antibiotics.

The researchers describe the entire pathway that Staph. aureus uses to burst open red blood cells, capture their hemoglobin, remove the iron-containing heme groups, transport them across the bacterial membrane and extract the iron. They also found that the human pathogens Anthrax and Listeria use the same method.

"It's a beautiful system, a complete and very elegant pathway," said Olaf Schneewind, M.D., Ph.D. professor of molecular genetics and cell biology, chairman of the committee on microbiology at the University of Chicago and director of the study. "It involves six different proteins, each with a specific function."

"Our findings could be used to develop drugs that would disrupt the Staphylococcal iron uptake systems," said co-author Eric Skaar, Ph.D., research associate in molecular genetics and cell biology at the University, "which could, in turn, prevent infection. Having the entire pathway provides us with multiple new drug targets."

With one known exception (Borrelia burgdorferi, the cause of Lyme disease), every pathogen must scavenge iron from its host in order to survive, grow and cause disease. Body fluids from humans and other mammals contain very little free iron, one of the most important defenses against infections. So bacteria have evolved specialized mechanisms to obtain iron from a host's body. Hemoglobin is the most abundent source of iron in the human.

Schneewind and colleagues found that the Staph. aureus genome contains a family of iron-regulated surface determinant (isd) genes that encode factors
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Contact: John Easton
jeaston@uchospitals.edu
773-702-6241
University of Chicago Medical Center
6-Feb-2003

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