Asthma and airway allergic responses are among the most common
chronic diseases in childhood affecting more than six million children in
the United States. The incidence and severity of asthma and allergies has been
increasing over the last two-three decades, affecting the general population
in terms of both morbidity and cost.
A research report published in the Journal of Leukocyte Biology shows that it may one-day be possible to reduce the incidence of asthma related to infection with respiratory syncytial virus (RSV). Specifically, the researchers found that a peptide, called STAT6-IP, when delivered to the lungs of neonatal mice at the time of first RSV exposure reduces the development of allergic-type lung inflammation and airway hyperresponsiveness ("twitchy" airways) in mice when they are "re-challenged" with RSV as young adults.
"Our data suggest that exposure to STAT6-IP has the potential to modulate long-term responses to allergens and microbial antigens implicated in the development of asthma," said Brian J. Ward, a researcher involved in the work and associate professor from McGill University Health Center, Research Institute in Montreal, Quebec, Canada.
To make their discovery, scientists infected mice with RSV, first as infants and then again as young adults. Mice were treated with STAT6-IP (or a control peptide) sprayed into the nose only at the time of the neonatal RSV infection. Following adult RSV re-infection, airway inflammation, hyperresponsiveness and structural changes were measured. The early-life STAT6-IP treatment did not prevent the mice from mounting an immune response to RSV and clearing the infection.
However, this treatment significantly reduced all of the asthma-like responses. Based on these findings, researchers investigated how STAT6-IP treatment changed the neonatal mouse response to RSV. They found that STAT6-IP prevented RSV-induced changes to airway cells called alveolar macrophages, which can promote asthma-like responses both during and following viral infections.
John Wherry, Deputy Editor of the Journal of Leukocyte Biology, said, "There has been a long-appreciated connection between early life RSV infection as subsequent asthma, but we have lacked the ability to influence this important early life 'imprinting' effect of RSV infection. These new results reveal new opportunities to think about recalibrating the immune-deviation caused by asthma-promoting RSV infection to reduce subsequent asthma and allergy."