Researchers have identified a protein that modifies the immune response to the flu and may also help reduce lung inflammation and improve survival during influenza.
The results — published in the journal Respiratory Research — suggest that the protein, GM-CSF, could be a potential therapeutic strategy for treating the flu, said E Scott Halstead, Assistant Professor at Penn State College of Medicine in Pennsylvania, US.
The researchers studied the survival and lung function of mice with influenza in the lab.
They found that the mice that had been given large amounts of a special cytokine — molecules that warn other cells that there is an infection or other trauma in the body — called GM-CSF, had better survival and lung function than the other mice.
“Previous research has shown that mice with naturally higher levels of GM-CSF might be protected from the flu. But in this study, we gave the mice GM-CSF after they got the flu, which is more similar to when a patient gets sick and then you do something to help them. Even after they got the virus, it still helped,” Halstead said.
While all viruses trigger a cytokine response in the body, Halstead said influenza tends to create a surge in a particular cytokine called type-2 interferon, which may be why influenza can be worse than other such viruses as rhinovirus or respiratory syncytial virus (RSV).
Type-2 interferon is associated with high levels of inflammation in the lungs.
The researchers also examined macrophages — a type of white blood cell found at sites of infection — from the mice’s lungs.
They sorted the macrophages into different populations and studied the genes the macrophages produced using a technique called RNA sequencing.
“We also saw that even though GM-CSF is thought to cause inflammation, in this study, we saw it doing the opposite,” Halstead said.
The researchers said that because they still saw the GM-CSF benefiting the mice several days after the mice had been infected with the flu, there is potential for using GM-CSF to treat flu and pneumonia in humans.