The new research from the University of Utah and Utah State University shows modulating the body's own inflammatory response to infection may help save more lives.
The researchers led by University of Utah Professor Dean Li discovered protecting blood vessels from hyper-inflammatory response to infection reduced mortality rates in mouse models of avian flu and sepsis by as much as 50 percent. Specifically, the researchers identified a protein signaling pathway, Robo4, when activated prevents inflammation from weakening blood vessels, which causes them to leak and can result in life-threatening organ damage.
The scientists said their findings raise the possibility of new broad-range therapies that could be rapidly implemented to fight both viral and bacterial infections, such as pandemic influenza and sepsis, and even potentially deadly human-made biological agents. Such therapies would be given along with antibiotics, antivirals, and other drugs.
"By blocking the ill effects of inflammation on the host or patient by stabilizing blood vessels, we have identified an entirely different strategy to treat these infections," Li said. "In essence, we've shown that rather than attacking the pathogen, we can target the host to help it to fight infections."
The study appears in the March 17 issue of Science Translational Medicine.