The research team wanted to determine whether blocking IL-17RA signaling would protect against acute lung injury following influenza infection. Using an influenza model in control and knockout mice (genetically engineered without IL-17RA), they worked to identify a pathway to control the function of IL-17RA and the migration and action of neutrophils. They found decreased levels of illness and death among the IL-17RA knockout mice, despite a higher viral load. The researchers found that the knockout mice had fewer neutrophils in the lung, thus lower levels of inflammation and less lung injury. Comparing their results to studies of IL-17RA knockout mice in other models of viral infection, the researchers conclude that therapeutic regulation of IL-17 signaling may be beneficial not only in acute lung injury, but also in treating viral infections of other organs.

"Each year, more than 200,000 people are hospitalized with flu-related complications in the United States," notes Dr. Kolls. "A number of those who have died from H1N1 flu this year have had lung damage different than we typically see with seasonal flu. These cases have been marked by deep lung infections with diffuse damage to the alveoli - the structures that deliver oxygen to the blood. Advancing our findings has the potential to benefit both."

Source: Louisiana State University Health Sciences Center