University of Central Florida Microbiology Professor Keith Ireton has uncovered a previously unknown mechanism that plays an important role in the spread of a deadly food-borne bacterium.
Listeria monocytogenes is a bacterium that can cause pregnant women to lose their fetuses and trigger fatal cases of meningitis in the elderly or people with compromised immune systems. The bacterium has been linked to outbreaks traced to food processing plants in the U.S. and Canada.
In 2002, a multi-state outbreak of listeriosis — the serious disease caused by Listeria — resulted in 46 confirmed cases, seven deaths and three stillbirths or miscarriages. Those cases in eight states were linked to people eating contaminated sliced turkey deli meat. From January to August 1985, there was another outbreak with 142 cases of listeriosis.
Scientists have long known that Listeria spreads from one human cell to another. Bacteria growing in one cell move fast enough to create a finger-like structure that protrudes from the cell and pushes into an adjacent cell. The bacteria then infect the adjacent cell.
Ireton and his team have discovered a previously unknown second process that aids in the spread of bacteria to healthy cells. The process, which gradually overwhelms the second cell’s ability to defend itself from infection, is featured in this week’s edition of the science journal Nature Cell Biology.
The plasma membrane, or outer layer, of healthy human cells normally exhibits tension. Such tension might be expected to prevent Listeria from spreading to adjacent uninfected cells. However, Ireton’s lab found that a Listeria protein called InlC appears to relieve tension at the plasma membrane in infected cells, making it easier for moving bacteria to deform the membrane and then spread into adjacent, healthy cells.
Ireton’s laboratory also reports that the way InlC relieves tension is by blocking the function of a human protein called Tuba. The normal role of Tuba in uninfected human cells appears to be to help generate tension at the plasma membrane. The Listeria protein InlC inactivates Tuba, reducing that tension and enabling bacteria to spread to nearby cells.
“The idea that a pathogenic bacterium can spread by controlling membrane tension in the human cell has not been previously described in the scientific literature,” Ireton said. “Our discovery could have relevance for bacterial pathogens that cause Shigellosis or Rocky Mountain spotted fever, as these bacteria resemble Listeria in their ability to move inside the host cell and spread.”
More research is needed, but Ireton says that discovering this mechanism could aid in future therapies and perhaps open a window into understanding how certain bacterial pathogens cause disease.
Others who worked on Ireton’s team include Tina Rajabian and Scott D. Gray-Owen at the University of Toronto, Balramakrishna Gavicherla at UCF and Martin Heisig, Stefanie Müller-Altrock and Werner Goebel at the University of Würzburg in Germany.
Ireton joined UCF’s Burnett School of Biomedical Sciences, housed in the College of Medicine, in 2006. He earned his Ph.D. at the Massachusetts Institute of Technology and completed post-doctoral work at the Pasteur Institute in France, a private institute dedicated to the treatment of diseases through biomedical research, education and public health. He conducted research and taught at the University of Toronto for several years before arriving at UCF.
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