Home Medizin Wissenschaftler der University of Louisville wollen Yersinia pestis, den Beulenpestbakterium, entwaffnen

Wissenschaftler der University of Louisville wollen Yersinia pestis, den Beulenpestbakterium, entwaffnen

von NFI Redaktion

When the body encounters bacteria, viruses, or harmful substances, its innate immune cells, neutrophils, gather at the site to fight off the intruder. However, bacteria and viruses have ways to evade these defenses. For example, the bacteria that cause bubonic and pneumonic plague, Yersinia pestis, can hide from the immune system and multiply in the body until they overwhelm the host. This ability allowed Y. pestis to spread the bubonic plague across Europe in the 14th century, resulting in the death of a third of the European population.

While the plague may not pose a serious threat to human health in modern times, researchers at the University of Louisville are studying Y. pestis to better understand its ability to evade the immune system and apply this understanding to combat other pathogens. Neutrophils, the immune system’s first responders, emit protein molecules to signal other neutrophils to attack and destroy the invader. Among the first molecules sent by neutrophils to signal an infection are leukotriene B4 (LTB4) lipid molecules. Y. pestis disrupts the immune response by suppressing the LTB4 signals.

“When you look at human plague, people don’t show symptoms immediately, even though they have an active infection, because the bacteria hide from the immune system. Then suddenly, there are a lot of bacteria, the immune system is overwhelmed, and in the case of pneumonic plague, the person dies of pneumonia,” said Matthew Lawrenz, Professor, UofL Department of Microbiology and Immunology.


Lawrenz’s research has received a new four-year, $2.9 million grant from the National Institutes of Health to examine how Y. pestis blocks LTB4. Ultimately, he expects this understanding to lead to ways to prevent Y. pestis from blocking the signals, and hopefully apply this understanding to other kinds of infections.

“This historical pathogen is really good at manipulating the immune system, so we’re using it as a tool to better understand how white blood cells such as neutrophils and macrophages respond to bacterial infections,” said Lawrenz. “In this project, we’re using Yersinia to better understand why LTB4 is so crucial in fighting the plague. This understanding would apply to almost any lung infection or other areas and could likely apply to viruses as well. As a member of the UofL Center for Predictive Medicine for Biodefense and Emerging Infectious Diseases, Lawrenz has been studying plague bacteria for nearly two decades.

Katelyn Sheneman, a doctoral student in Lawrenz’s lab, has also received a prestigious $100,000 NIH research fellowship to fund her research on how Y. pestis alters the content of extracellular vesicles, cellular containers produced by immune cells containing proteins, lipids like LTB4, and other components. These vesicles are released into the bloodstream to inform other cells about what is happening in their part of the body, such as an infection.

“My project is looking at how Y. pestis alters the number of vesicles produced, what is packaged inside them, and how other cells respond to them,” said Sheneman. “We have some good evidence that Y. pestis is able to manipulate the production of these vesicles, so we’ll be investigating the role of the vesicles in lung infections and how this influence contributes to the overall systemic infection.”

As there is no effective vaccine against infection by Y. pestis, and it has the potential to be used as a bioweapon, Lawrenz and Sheneman study Y. pestis in the biosafety level 3 facilities of the UofL Regional Biocontainment Laboratory, part of a network of twelve regional and two national biocontainment laboratories for investigating infectious agents. Biosafety level 3 facilities are built according to stringent federal security standards to protect researchers and the public from exposure to the studied pathogens.

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