Cause of Flu Fatalities Pinpointed by Researchers
While illnesses such as influenza are often little more than an inconvenience, sometimes they can become fatal, and now researchers at the Scripps Research Institute claim to have found out why that can happen.
Writing in Friday’s edition of the journal Cell, the Scripps scientists discovered the source of the severer immune-system reaction known as a “cytokine storm,” which “floods the tiny air sacs of the lungs with fluid and infection-fighting cells, blocking off airways and damaging body tissues and organs,” the Institute said in a September 15 press release.
According to the researchers, viruses (including influenza) typically destroy cells that line the alveoli–tiny air sacs responsible for exchanging gases in the lung. To combat this, the body creates small cell-signaling proteins known as cytokines. The cytokine storm phenomenon occurs when the body produces too many of those molecules, and the Scripps team has pinpointed the cause.
“Using advanced chemical and genetic approaches that allow tracking and modulation of receptor function in real time, the Scripps Research team set out to determine the role of a receptor S1P1 (molecule on the surface of a cell that binds to molecules, triggering a certain biological effect) for a specific molecule known as Sphingosine-1-phosphate (S1P),” they wrote in the press release.
“S1P1 has been a topic of investigation“¦ due to its connection to autoimmune disease,” the Scripps researchers added. “Unexpectedly, the team found that manipulating the S1P1 receptors in the endothelial cells–the thin layer of cells lining the interior surface of blood vessels–in the lung affected cytokine release. Previously, scientists had assumed that cytokine release occurred through virus-infected cells or other cells lining the lungs.”
In a separate press release, Cell Press, publishers of the journal where the paper detailing the Institute’s work appears, said that this discovery could offer “a life-saving new line of defense” by preventing an infected individual’s body from harming itself. Furthermore, they noted that this method will not affect the virus itself, thus not putting “pressure” on it “to adapt and develop drug resistance.”
“In mice treated with a molecule that targets S1P1, cytokine production and the early signs of inflammation are suppressed,” Cell Press noted. “As a result, the animals are much more likely to survive infection with H1N1 swine flu virus.”
Researchers noted that clinical trials of S1P1-targeting drugs were currently underway at multiple pharmaceutical companies, including Novartis, Actelion, and Receptos.
John Teijaro and Kevin Walsh of Scripps Research Institute were credited as the lead authors of the study, with their colleagues Stuart Cahalan, Daniel M. Fremgen, Edward Roberts, Fiona L. Scott, Esther Martinborough, and Robert J. Peach also credited as authors.
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