The laboratory of Dr. Christopher Lupfer, assistant professor of biology, recently published a paper on secondary infections.
Several people contributed to this research, including:
- Graduate students in Lupfer’s lab
- Researchers at the University of Tennessee Health Sciences Center
- Researchers at St. Jude Children’s Research Hospital
- Cox Hospital
He and his collaborators explored how the flu can become something much worse. How do we stop that from happening?
About his paper
The flu weakens your immune system. Bacteria sees this and takes advantage of it. Now you’re fighting two infections.
When you’re fighting an infection, your body sends out immune proteins called cytokines. When it’s overwhelmed with two infections, the body goes into overdrive. It produces too much of the cytokines, causing too much inflammation.
“Secondary infections are common and severe, especially in elderly flu patients,” Lupfer said. “By understanding the immune response to secondary infections, we can hopefully develop better treatments that can reduce hospital stays and save lives.”
Lupfer’s research looks at why there is so much inflammation in secondary infections. Luper’s collaborative team also investigates if decreasing the inflammation can help the people with two infections recover.
In addition, their research looked at what would happen if fewer immune proteins were made during secondary infections. Specifically, they look at the IL-1β protein. They discovered that less IL-1β led to a quicker recovery.
One interesting find in Lupfer’s studies includes how the bacteria uses inflammation. In a secondary infection, the bacteria uses inflammation to travel from the lungs to the brain, making the infection worse.
“By decreasing the amount of IL-1β and inflammation, we may be able to prevent or reduce the amount of bacteria in the brain and help patients recover faster,” Lupfer said.
Lupfer’s paper is entitled “Enhanced IL-1β production is mediated by a TLR2-MYD88-NLRP3 signaling axis during coinfection with influenza A virus and Streptococcus pneumoniae.” It was published in the journal PLOS One.