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Bubonic plague kills by cutting off cellular communication

Bubonic plague kills by cutting off cellular communication, say U-M scientists.

One molecule holds the key to plague's lethal effects.

ANN ARBOR --- Yersinia pestis, the deadly bacterium that causes bubonic plague, kills by cutting off a cell's ability to communicate with other immune system cells needed to fight off the bacterial invasion. In a study published in the Sept. 17 issue of Science, University of Michigan scientists identify one protein responsible for the plague's lethal effect and the molecular family it targets.

"Yersinia is a clever pathogen," says Kim Orth, Ph.D., a research investigator in the U-M Medical School. "It found our Achilles heel --- one family of molecules used by every mammalian cell to transmit signals involved in the immune response and cell death."

If scientists can understand the mechanism Yersinia uses to control cell signaling and how it destroys the immune communications system, it could have important implications in medicine, especially in cancer and immune-related diseases, Orth adds.

"YopJ, the protein Yersinia uses to block this signaling process, is one of six proteins injected by the bacteria into immune cells called macrophages," says Jack E. Dixon, the Minor J. Coon Professor of Biological Chemistry in the U-M Medical School, who directed the research. Every Yop has a specific function and they work together to gain entry into a cell and destroy the body's defense systems.

"In this study, we found that YopJ binds to similar molecules located at the same point in two critical cellular signaling pathways," Dixon says.

The first pathway, called MAPK, controls cell growth and regulates the immune inflammatory response. The second pathway, known as NFkB, also regulates the immune inflammatory response, as well as preventing cell death and controlling embryonic development.

"Scientists thought these
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Contact: Sally Pobojewski
pobo@umich.edu
734-647-1844
University of Michigan
16-Sep-1999


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