University of Central Florida
09/12/2024 | Press release | Distributed by Public on 09/13/2024 09:53
Med School Scientist Receives Prestigious NSF Award for Inflammation Research
A College of Medicine researcher has received a prestigious U.S. National Science Foundation CAREER Award to support her research into the cellular causes of inflammation, discoveries that could be pivotal for treating conditions like Crohn's disease and arthritis.
Justine Tigno-Aranjuez's lab has been researching lipid mediators - bioactive lipids the body produces in response to stimuli such as microorganisms or microbial products. Scientists have long known that lipid mediators can influence both the initiation and resolution of inflammation. However, the exact mechanisms by which this happens are still not completely understood.
She will use her five-year grant of more than $1 million to study how a specific receptor and cellular signaling pathway, known as NOD2, influences the production of lipid mediators with the goal of better understanding its impact on inflammation.
"The NOD2 pathway has been widely studied, in part, because of its well-known genetic links with inflammatory diseases like Crohn's Disease and Early Onset Sarcoidosis," Tigno-Aranjuez says. "Most of the focus has been on the events which promote the production of inflammatory cytokines, another type of protein-based signaling molecule. There are very few studies looking into how exactly activation of the NOD2 pathway can lead to the production of lipid mediators. Our hope is that by understanding the molecular events important for the production of such lipid mediators, we can guide therapies in the future that either prevent inflammation or promote its resolution."
Today, nearly 35% of US adults suffer from chronic inflammatory disease. Inflammation occurs as a part of the body's natural immune response. When a foreign substance like a virus or bacterium enters your body, it cues production of cytokines and lipid mediators that recruit inflammatory cells to control the infection. Later, the body produces other to promote healing and the clearance of dead cells.
However, if the body incorrectly starts inflammation when no foreign object is present, or doesn't stop the inflammatory process once the danger is over, patients can develop chronic illness.
"In the past, researchers believed that when something caused inflammation, let's say you get poked with something or infected with a microbe, when you take that away, everything will go back to normal," Tigno-Aranjuez says. "But what researchers have found out is there are a lot of factors that go into bringing us back to baseline, including the active production of certain classes of lipid mediators and that's why it's important that we understand how they are produced."
Every year, hundreds of researchers apply for the NSF's CAREER Award which support early-career faculty who they see as potential role models in education and research. With only about 50 given out this year, Tigno-Aranjuez says she was honored and grateful for the award.
"This was one of my long-standing pet projects. It wasn't the original focus of the lab when I started, but it was something that I was really interested in pursuing and taking further. So, to see it now funded and recognized is really important." she says.
This grant will also offer UCF undergraduates a sustained research experience to prepare them for future careers in the sciences and in medicine.
"The grant will support a Sustained Research Initiative, which I am hoping will open up a lot of opportunities for undergraduates to get hands-on research in a controlled setting." she says. "Students will be working both as individuals and as a team in research labs, and, if they do really well, will have the opportunity to serve as an instructor for future students."
Tigno-Aranjuez immigrated to the United States from the Philippines to conduct her graduate and postdoctoral training at Case Western Reserve University in Cleveland. She joined UCF in 2015 and focuses her research on innate immune signaling pathways involved in chronic inflammatory diseases.