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Analyzing Cell Death * Plague Protein Stalls Cell Death, Speeds Host Death

Any common themes that emerge among disparate infectious processes
could point investigator to fruitful lines of inquiry. At least, such thinking
helped motivate scientists at Northwestern University. Led by Wyndham
Lathem, Ph.D., assistant professor in microbiology-immunology, a team of
researchers at Northwestern has been studying Y. pestis for years.
Back in 2007, they demonstrated that the presence of a protein called
the plasminogen activator protease (Pla) is required for Y. pestis to live inside
the lungs. And now, as a result of more recent work, they have determined
that Pla shuts down a molecule, Fas ligand (FasL), which stimulates a form
of programmed cell death known as apoptosis. The result is a disrupted
immune response during infection. This allows Y. pestis to overwhelm the
lungs, causing death.
"This is the first time anyone has shown how bacteria can subvert
apoptotic cell death by directly destroying Fas ligand," said Dr. Lathem.
Dr. Lathem and colleagues described their work April 9 in Cell Host &
Microbe, in an article entitled "The Pla Protease of Yersinia pestis Degrades
Fas Ligand to Manipulate Host Cell Death and Inflammation." This article
describes how they added Pla to glass slides with various fluorescently tagged
proteins. If the protease showed an affinity for a specific protein, it would
chew off pieces, making it appear less florescent when viewed under a
microscope.
"We knew that Pla must be chopping up host proteins in some manner
and we looked to discover exactly what proteins were being affected," said
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| GENengnews.com

A scanning electron micrograph depicting a mass of Yersinia pestis bacteria.
Rocky Mountain Laboratories, NIAID, NIH
http://www.GENengnews.com
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